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1 Optimization of a Type Three Secretion System-based P. aeruginosa live vector for antigen delivery Running title: optimization of TTSS-based P. aeruginosa vaccine vector Authors: Olivier EPAULARD, Madiha DEROUAZI, Carole MARGERIT, Raphaël MARLU, Didier FILOPON, Benoît POLACK*, Bertrand TOUSSAINT Address (for all authors): TIMC-TheREx (UMR5525 CNRS-UJF) Bâtiment Jean Roget - 8 th floor UFR de Médecine Université Joseph Fourier Grenoble 1 38706 La Tronche Cedex FRANCE * Corresponding author: Benoît POLACK DPBC-Enzymologie CHU de Grenoble – BP217 38043 GRENOBLE cedex09 FRANCE [email protected] . Tel +33 4 76 76 54 87; fax +33 4 76 76 59 35 ACCEPTED Copyright © 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved. Clin. Vaccine Immunol. doi:10.1128/CVI.00278-07 CVI Accepts, published online ahead of print on 19 December 2007 on September 9, 2018 by guest http://cvi.asm.org/ Downloaded from

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Optimization of a Type Three Secretion System-based P.

aeruginosa live vector for antigen delivery

Running title: optimization of TTSS-based P. aeruginosa vaccine vector

Authors:

Olivier EPAULARD, Madiha DEROUAZI, Carole MARGERIT, Raphaël MARLU,

Didier FILOPON, Benoît POLACK*, Bertrand TOUSSAINT

Address (for all authors):

TIMC-TheREx (UMR5525 CNRS-UJF)

Bâtiment Jean Roget - 8th

floor

UFR de Médecine

Université Joseph Fourier Grenoble 1

38706 La Tronche Cedex

FRANCE

* Corresponding author:

Benoît POLACK

DPBC-Enzymologie

CHU de Grenoble – BP217

38043 GRENOBLE cedex09

FRANCE

[email protected].

Tel +33 4 76 76 54 87; fax +33 4 76 76 59 35

ACCEPTED

Copyright © 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.Clin. Vaccine Immunol. doi:10.1128/CVI.00278-07 CVI Accepts, published online ahead of print on 19 December 2007

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Abstract 1

During the last years, the use of type III secretion system-based bacterial vectors for 2

immunotherapy purpose has been assessed in various applications. We showed that a type 3

III secretion-based P. aeruginosa vector delivering the OVA antigen induced an efficient 4

specific CD8+ T lymphocyte immune response against OVA-expressing cells. Because of 5

the intrinsic toxicity of the vector, further virulence attenuation was needed. Therefore, we 6

explored the effect of the deletion of quorum sensing genes and aroA gene toward toxicity 7

and efficiency of the vector strain. AroA mutation of our strain (making the strain 8

auxotrophic for aromatic aminoacids) conferred a strikingly reduced toxicity, with a 9

bacteria lethal dose more than 100 times higher than with the parental strain. Quorum 10

sensing gene mutation alone was associated with a slightly reduced toxicity. In a 11

prophylactic OVA-expressing melanoma mouse model, OVA-delivering aroA-deficient 12

mutant was the most efficient at low dose (105), but dose enhancement was not associated 13

with greater immune response. Quorum-sensing deficient strain was the most efficient at 14

mild dose (106), but this dose was close to the toxic dose. Combination of both mutations 15

conferred the highest efficiency at elevated dose (107), in agreement with known negative 16

effects of quorum-sensing molecules upon T cell activation. In conclusion, we have 17

obtained a promising immunotherapy vector regarding to toxicity and efficiency for further 18

developments in both anti-tumour and anti-infectious strategies. 19

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The use of live bacteria and bacterial virulence factors as therapeutic tools in 1

human medicine has been considered for more than a century. The observation that the 2

onset of a bacterial infection could modify the course of a malignant disease (6) was a 3

hallmark in this history, but very few procedures (such as the intra-vesical administration 4

of an attenuated Mycobacterium bovis strain for the cure of non-invasive urothelial 5

carcinoma) had been finally used in routine. In the last 10 years, better characterization of 6

bacterial devices (mainly toxins and secretion systems) and extensive progresses in 7

genomic studies allowed engineering of bacteria (mainly E. coli and Salmonella spp). 8

These domesticated agents can be delivered to mammals organisms for different purposes. 9

Notably, the design of antigen-delivering bacteria triggering antigen-specific cytotoxic 10

CD8+ T lymphocyte response is an emerging investigation field in vaccine development 11

(5). Antigen delivery can be performed by using intrinsic properties of bacterial toxins (as 12

with Listeria monocytogenes-derived vector (20) or secretion pathways normally used by 13

bacteria to release toxins, such as type III secretion system (TTSS). This system was 14

considered promising because it allows Gram-negative rods to inject toxins within 15

eukaryotic cell cytoplasm; therefore, epitopes delivered by this system were likely to be 16

presented by antigen-presenting cells MHC-I molecules, and to activate cytotoxic T 17

lymphocytes. Moreover, the bacteria-associated, toll-like receptor-mediated danger signals 18

would ensure the correct activation of antigen-presenting cells. Previous works showed 19

that antigen-delivering TTSS-based Yersinia (23) and Salmonella (15) vectors can be used 20

in anti-microbial and anti-tumoral immunotherapy, and induced simultaneous CD4 and 21

CD8 antigen-specific lymphocytes (16). We recently showed that a TTSS-based 22

Pseudomonas aeruginosa vector efficiently induced an antigen-specific CD8+ T cell 23

response and could be exploited in anti-tumour immunotherapy (8). The application field 24

of these antigen-delivering vectors may be very large, and diverse disorders such as cancer, 25

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HIV infection or malaria are likely to be prevented or treated by microbe-based 26

immunotherapy (12). 27

One limitation to the use of such vectors is their intrinsic toxicity. We had used a P. 28

aeruginosa strain carrying deletions in the genes of the TTSS toxins exoenzymes ExoS and 29

ExoT and spontaneously ExoU negative (strain CHA-OST), but toxicity reduction was yet 30

to be optimized. Here, we present the results concerning the toxicity and the efficiency 31

obtained with much more attenuated P. aeruginosa TTSS-based vectors in an anti-tumour 32

model. 33

34

MATERIAL AND METHODS 35

Bacterial strains. CHA-OST, a ∆exoS, ∆orf1 and ∆exoT Pseudomonas aeruginosa strain, 36

has been previously described (19). Additional deletions of aroA, lasI and rhlI were 37

performed in CHA-OST using the Cre-lox system that we previously adapted to P. 38

aeruginosa. This system allows performing multiple successive allelic exchanges in the 39

same strain (19). The genes lasI and rhlI encoding synthases of the QS homoserine-40

lactones (HSL) (respectively 3-oxo-C12-HSL and C4-HSL) and the gene aroA were 41

deleted by allelic exchange (see primer sequence in table 1). We generated three attenuated 42

mutants from CHA-OST: CHA-OA (∆exoS ∆orf1 ∆exoT ∆aroA), CHA-OAL (∆exoS ∆orf1 43

∆exoT ∆aroA ∆lasI), and CHA-ORL (∆exoS ∆orf1 ∆exoT ∆rhlI ∆lasI). Growth kinetic 44

assays were performed in Luria-Bertani (LB) broth or Vogel-Bonner (VB) minimal broth 45

by measuring optic density at 600 nm. 46

Plasmids and TTSS assay 47

Production and delivery of non-bacterial proteins by TTSS is obtained by 48

transforming P. aeruginosa strains with plasmids pS54-Ova_ExsAi (to obtain ovalbumin 49

delivery) or pS54-GFP_ExsAi (to obtain green fluorescent protein (GFP) delivery). Briefly, 50

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these previously described plasmids (8) encode a traductional fusion between an optimized 51

ExoS fragment (ExoS first 54 aminoacids, ExoS54) and ovalbumin (C-terminal fragment) 52

or GFP, under the control of ExoS native promoter, and exsA gene encoding the ExoS 53

transcriptional activator cloned under the control of an isopropyl-β-D-54

thiogalactopyranoside (IPTG) inducible promoter. Strains transformed with these plasmids 55

produce the fusion protein (S54-GFP or S54-Ova) when cultivated with IPTG; TTSS-56

mediated secretion of fusion protein is obtained by calcium depletion or eukaryotic cell 57

contact. Plasmid propagation is ensured by cultivating bacteria with 300 mg/l carbenicillin. 58

Strains transformed by either pS54-Ova_ExsAi or pS54-GFP_ExsAi were cultivated 59

from an OD600 of 0.2 in LB broth supplemented with 0.8 mM IPTG, and/or 5 mM EGTA 60

and 20 mM MgCl2 until they reached an OD600 of 1 to 2. ExoS54-fused GFP production 61

was assessed in pellet after centrifugation and was expressed as the ratio of fluorescence 62

intensity by OD600. ExsoS54-fused ovalbumin secretion was assessed in supernatant after 63

centrifugation by 10% trichloroacetic acid protein precipitation and SDS-PAGE analysis. 64

For immunization control, CHA-OST strain was transformed with plasmid 65

pExsAind. This previously described plasmid (9) contains the already mentioned ExsA-66

inducible system without any fusion protein. 67

Mice 68

Female C57BL/6 mice were purchased from Janvier SA (Le Genest-Saint-Isle, 69

France) and used at 6-8 weeks of age. Experiments were approved by the Université J. 70

Fourier committee for animal experimentation. 71

Vector injection 72

Bacteria were grown in LB broth supplemented with 300 mg/l carbecillin and 0.8 73

mM IPTG from an OD600 of 0.2 to an OD600 of 1.5, and then resuspended in PBS before a 74

100 µl subcutaneous injection in mouse right flank. 75

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Mammalian cell lines 76

B16-OVA is a melanoma cell line from C57BL/6 mice constitutively expressing 77

ovalbumin (3) and cultivated in medium supplemented with 500 mg/l geneticin. 78

Tumour challenge 79

2.105 B16-OVA cells were injected subcutaneously in mouse left tight. Tumour 80

size was assessed every two days. Mice were sacrificed when the tumour diameter reached 81

1 cm. 82

83

RESULTS 84

Determination of time schedule 85

Using partially attenuated CHA-OST strain, we determined which injection dates 86

were more appropriate in a two-injection schedule. Mice received subcutaneously 2.105 87

B16-OVA cells at day 0 and were injected with 106 ovalbumin-delivering CHA-OST either 88

at days -14 and -7, at days -7 and 0, at days 0 and +7, or at days +7 and +14. As a negative 89

control, another group received 106 CHA-OST not delivering any antigen at days -14 and -90

7. Mice injected with the “days -14 and -7” schedule demonstrated the best protection, 91

with more than 80% of animals remaining tumour-free (fig. 1); therefore, following 92

experiments with more attenuated strains were performed identically (unless mentioned). 93

Generation of attenuated vectors 94

Target genes for further virulence attenuation were aroA and two genes 95

participating in quorum sensing (QS) system, lasI and rhlI. AroA-encoded 3-96

phosphoshikimate 1-carboxyvinyltransferase is a key enzyme in aromatic aminoacid 97

synthesis; the aroA deletion conferred auxotrophy for aromatic aminoacids and was 98

successfully used to elaborate attenuated P. aeruginosa strains for purpose of anti-99

Pseudomonas vaccination (18). LasI and rhlI encode the two enzymes producing QS 100

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homoserine lactones [respectively N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C12-101

HSL) and N-butanoyl-homoserine lactone (C4-HSL)]; P. aeruginosa QS inactivation was 102

associated with virulence attenuation in various animal models such as pneumonia (13,17), 103

burns (22), or pyelonephritis (14). 104

We used the Cre-lox system that we previously adapted to Pseudomonas 105

aeruginosa (19). By successive mutations, we generated three attenuated mutants from 106

CHA-OST: CHA-OA (∆exoS ∆exoT ∆aroA), CHA-OAL (∆exoS ∆exoT ∆aroA ∆LasI), and 107

CHA-ORL (∆exoS ∆exoT ∆rhlI ∆lasI). All mutants were genetically verified by PCR (data 108

not shown) and then phenotypically for growth rates and TTSS function. 109

In vitro characterization of attenuated vectors 110

As aroA deletion was previously reported to confer reduction of growth rates, we 111

measured the growth of CHA-OST, CHA-OA, CHA-OAL and CHA-ORL mutant in 112

Luria-Bertani (LB) rich medium and Vogel-Bonner (VB) minimal medium and observed 113

that CHA-OA and CHA-OAL grow slower than CHA-OST and CHA-ORL in both media 114

(table 2). This phenotype resulting from aroA deletion was likely to be associated with 115

reduced in vivo toxicity, but could also result in TTSS deficiency. 116

We therefore compared the in vitro TTSS efficiency of the four strains. We 117

obtained transformants with plasmid pS54-GFP_ExsAind or pS54-Ova_ExsAind and 118

assessed the production and secretion by TTSS of ExoS54-fused proteins by the different 119

strains. We used four growth conditions in LB medium: no TTSS stimulation; TTSS 120

stimulation by calcium depletion induced by 5 mM EGTA (triggering production and 121

secretion of ExoS54-fused protein); exsA transcription induction by 0.8 mM IPTG 122

(triggering only production of ExoS54-fused protein); and supplementation with both 123

EGTA and IPTG. 124

ExoS54-GFP production was assessed by measuring fluorescence in culture pellet 125

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of pS54-Ova_ExsAi transformants. We observed (fig. 2A) that mutants CHA-ORL, -OA 126

and -OAL demonstrate identical (ORL) or even higher (OA, OAL) GFP production levels 127

when compared to CHA-OST or wild type CHA strain. This feature was promising for 128

TTSS-based immunotherapy. The same results were obtained when assessing TTSS-129

mediated secretion of ExoS54-Ova by SDS-PAGE (we did not assessed secretion of 130

ExoS54-GFP secretion by fluorimetry because of Luria-Bertani broth high background 131

fluorescence). Mutants CHA-ORL, -OA and -OAL secrete identical or higher amount of 132

the fusion protein when compared with CHA-OST and wild type CHA (fig. 2B). This 133

indicates that although the growth of aroA-deleted strains is affected, TTSS function is 134

maintained. 135

In vivo toxicity of attenuated mutants 136

We then assessed the in vivo toxicity of these different strains by observing 137

mortality after one subcutaneous injection of 105, 10

6, or 10

7 ovalbumin-delivering bacteria 138

to 6 weeks old female C57BL/6 mice (fig. 3A). The pS54-Ova_ExsAi transformed bacteria 139

were grown in medium containing 300 mg/l carbecillin and 0.8 mM IPTG from a OD600 140

0.2 to a OD600 between 1 and 2. When injecting 107 bacteria, 4/6 mice injected with CHA-141

OST and 1/6 mice injected with CHA-ORL died in the first 40 hours. No death was 142

observed in the groups vaccinated with 107 CHA-OA or CHA-OAL, or in other groups 143

vaccinated with 105 or 10

6 bacteria. We then assessed the letality of doses 10

8 and 10

9 for 144

CHA-ORL, CHA-OA and CHA-OAL; all the mice injected with strain CHA-ORL died at 145

both doses, meanwhile all the mice injected with CHA-OA and CHA-OAL remained alive. 146

Therefore, these different mutants demonstrate a partially (CHA-ORL) or greatly (CHA-147

OA and CHA-OAL) reduced in vivo toxicity. 148

In vivo efficiency of attenuated mutants 149

We then assessed the antigen delivery efficiency of these vectors in a mouse model 150

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of prophylactic immunotherapy assay using syngenic B16 melanoma cells expressing the 151

ovalbumin as a model antigen (B16-OVA cell line). Surviving mice from the previous 152

experiment (105, 10

6 and 10

7 groups) were subcutaneously injected with an identical dose 153

of the same ovalbumin-delivering P. aeruginosa strain at day 8 (to complete the two-154

injection schedule), and a subcutaneous injection (in a different site) of 2.105 B16-OVA 155

cells was performed at day 15. One more group received 2 injections of CHA-OST not 156

delivering ovalbumin as a negative control before tumour challenge. Mice were sacrificed 157

when tumour diameter reached 1 cm. As we demonstrated it previously, the ability of the 158

vector to induce an efficient anti-ovalbumin cellular immune response is associated with 159

the inhibition of the onset of the tumour. 160

We observed contrasted dose-dependant efficiency (fig. 3B). For the lowest vector 161

dose (105), CHA-OST and CHA-ORL demonstrate mild tumour growth inhibition, and 162

CHA-OA and CHA-OAL had a respectively better and lower efficiency. At mild dose 163

(106), protection was almost complete or complete for respectively CHA-OST and CHA-164

ORL; CHA-OAL showed an improved efficiency, and CHA-OA efficiency was 165

comparable with previous dose. At the highest dose (107), CHA-OAL showed an almost 166

complete protection, and CHA-ORL and CHA-OA a respectively comparable or lower 167

efficiency; the two surviving mice injected with 107 CHA-OST did not develop tumour. 168

Influence of modification of injection schedule 169

We explored the influence of immunization schedule (dose and frequency) upon the 170

efficiency of the most attenuated vector, CHA-OAL, in the prophylactic anti-B16-OVA 171

assay. The following conditions were assessed: one injection of either 105 or 10

6 bacteria 172

at day 1 and 8; either one or two injection(s) of 105 bacteria at day 1, 4, 7, 10, and 13; and 173

either one or two injection(s) of 106 bacteria at day 1, 4, 7, 10, and 13. Tumour challenge 174

was performed at day 15. 175

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Table 3 shows the proportion of tumour-free mice at day 45. We observed the same 176

relation between dose and efficiency, and that vaccination schedule (2 or 5 injections) of 177

the same total dose (106 or 10

7) has no influence upon protection. Indeed, mice injected 178

with a total dose of 106 bacteria were not protected, and mice vaccinated with a total dose 179

of 5.106 or 10

7 were almost all protected; splitting the total dose in 2 or 5 injections did not 180

influence the anti-tumour protection. 181

182

DISCUSSION 183

The aim of this study was to generate mutants of our P. aeruginosa strain with 184

reduced toxicity and conserved or enhanced efficiency for immunotherapy purpose. We 185

choose two different mutagenesis targets: aromatic aminoacids (AAA) metabolism and QS 186

system. 187

Auxotrophic strains (notably for AAA) have been generated to obtain attenuated 188

vaccine strains in mammals (1,4,10) and fish (25) to trigger protective anti-bacterial 189

response, and in immunotherapy studies to obtain safer vectors (15). Our ∆aroA mutants 190

(CHA-OA and CHA-OAL) have reduced growth rates in LB and VB media, and the 191

dramatic mortality reduction observed when injecting high amounts of these strains in 192

C57BL/6 mice is likely to be related with a low multiplication in host, allowing 193

elimination of the bacteria. However, several works have demonstrated the link between 194

metabolic processes and virulence in prokaryotes, notably for TTSS (7). Therefore, the low 195

toxicity of our mutants could have been also related to a low virulence because of a 196

decrease in TTSS functions. Contrarily, in vitro study of strains transformed with plasmids 197

pS54-Ova_ExsAi or pS54-GFP_ExsAi showed for both ExoS54-fused proteins an 198

enhanced type III production or secretion level, demonstrating that toxicity reduction was 199

not due to TTSS inactivation, but mainly to low replication capacity inside mice. The good 200

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results observed when assessing the performances as immunotherapy vectors of the two 201

∆aroA strains are due to this interesting association of poor replication and enhanced TTSS 202

levels. 203

Considering QS system inactivation, previous experiments had shown that it 204

conferred a reduced virulence in various models, in accordance with the role of QS 205

signalization of many virulence factors of P. aeruginosa. Several works (2,11) assessed 206

that production of 3-oxo-C12-HSL and C4-HSL induced a down-regulation of TTSS level, 207

as observed when bacterial density is high. Therefore, rhlI and/or lasI mutations were 208

likely to be associated with greater, or at least unchanged, TTS levels when compared with 209

parental strain; this was confirmed when measuring S54-GFP production or S54-Ova 210

secretion by CHA-ORL and CHA-OAL. Moreover, it has been demonstrated that HSLs 211

display pleiotropic activity upon immune system, particularly macrophages and T 212

lymphocytes. Indeed, IFN-γ secretion by T lymphocytes after antigen-specific stimulation 213

is decreased when cells are incubated with 3-oxo-C12-HSL (21); and the same HSL 214

display a negative influence upon T lymphocyte proliferation after concanavaline A 215

activation (24). This may explain why ∆lasI vector CHA-OAL displayed better results at 216

high doses (107) than CHA-OA. The use of this mutant may be associated with no down-217

regulation of CD8+ T lymphocyte response, and therefore a better destruction of targeted 218

cells. 219

Besides, it is noteworthy that aroA mutation, by altering the production of aromatic 220

aminoacids, may influence the synthesis of signal molecules important for virulence of P. 221

aeruginosa (27). 222

To summarize, aroA mutation is likely to confer a higher TTSS functional level and 223

a greatly reduced toxicity, in relation with a reduced intra-host multiplication; and QS 224

mutation is likely to confer a slight reduced toxicity and a reduced negative effect of QS 225

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molecule upon immune system. 226

Taken together, these results may lead to choose CHA-OAL for further 227

developments. Indeed, CHA-ORL demonstrated the highest efficiency for a non-letal dose 228

(complete anti-tumour protection at 106), but toxicity reduction was mild. CHA-OA has a 229

strikingly reduced letality, and demonstrated efficiency at low dose (105); this great 230

therapeutical index was a key property for further development. However, its efficiency is 231

lower than CHA-ORL and CHA-OAL at higher doses. CHA-OAL shares the same toxicity 232

reduction than CHA-OA, but demonstrated a better efficiency at high doses. This 233

maximally attenuated strain may represent the best compromise between virulence 234

attenuation and efficiency. 235

Moreover, the exploration of various injection schedules (modification of dose and 236

frequency) using CHA-OAL showed that 2 injections were enough to obtain an important 237

protection, and that it was not necessary to split the total dose in more injections. This 238

simplicity is also an argument to consider this strain for immunotherapy purpose. 239

240

ACKNOWLEDGMENTS. 241

This work was supported by grants from the Association pour la Recherche contre 242

le Cancer (ARC) and from the Agence Nationale de la Recherche ("Emergence et 243

Maturation de Projets de biotechnologie" BacVac 2007). 244

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Table legend

Table 1: primer sequence for the PCR fragments used in allelic exchange for the deletion

of genes aroA, lasI and rhlI.

Table 2: growth kinetics of mutants CHA-OST, CHA-ORL, CHA-OA and CHA-OAL in

Luria-Bertani (LB) and Vogel-Bonner (VB) broths: doubling time.

Table 3: anti-tumour protection after prophylactic vaccination using S54-Ova delivering

CHA-OAL at different schedules and doses: proportion of tumour-free mice at day 45. NC:

negative control (CHA-OST not delivering any antigen).

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Figure legend

Figure 1: determination of best time schedule for vaccination using strain CHA-OST. Mice

received the same dose of ovalbumin-delivering CHA-OST with different delay from

tumour implantation (Day 0): at day -14 and -7; at day -7 and 0; at day 0 and day +7; or at

day +7 and +14. A day -14 and day -7 schedule using a CHA-OST strain delivering no

antigen was used as a negative control. Mice were sacrificed when tumour diameter

reached 1 cm.

Figure 2: in vitro TTSS efficiency of the mutants. A) fluorescence intensity in culture

pellet of wild type (WT) strain and different mutants transformed by plasmid pS54-

GFP_ExsAi with different TTSS-activating conditions. Negative control: CHA-OST

without plasmid. Error bars: one standard error. B) SDS-PAGE analysis of secretion of

S54-Ova by WT strain and different mutants transformed by plasmid pS54-Ova_Exsai.

Culture medium was supplemented with both IPTG and EGTA. Negative control: CHA-

OST without plasmid.

Figure 3: in vivo toxicity (A) and efficiency (B) of TTSS-based mutant vectors. A) mouse

mortality after SC injection of mutants at doses 105, 10

6, 10

7, 10

8 or 10

9. B) survival after

tumour implantation in mice vaccinated beforehand twice by 105 (thick pale grey line), 10

6

(thick dark grey line) or 107 (thick black line) mutant delivering S54-Ova: CHA-OST,

CHA-ORL, CHA-OA, and CHA-OAL. Negative control: 106 CHA-OST not delivering

S54-Ova (thin line).

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Table 1: primer sequence for the PCR fragments used in allelic exchange for the deletion

of genes aroA, lasI and rhlI.

Primer sequence

Gene

5’ flanking region of the gene 3’ flanking region of the gene

aroA Forward: GCCGATTGTGCTAACCGCG Reverse: AGCCCTCCACTTCGGTGGT

Forward: CGCTCATGTTCATACCTGTAG Reverse: TACGACATGCCGATGGCCAG

lasI Forward: AAGTGGCTATGTCGCCG Reverse: AGTTTTTTATCGAACTCTTCGCGC

Forward: GGCCTGGACGTATCGCG Reverse: CTTAAGGAGTCGGACGGG

rhlI Forward: GCTCGGCGATCATGGCG Reverse: CGCGGTGCGCCGCAAGG

Forward: TGTCCGGAAATCCTCATGC Reverse: GCGTCATCGGGCGTTCC

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Table 2: growth kinetics of mutants CHA-OST, CHA-ORL, CHA-OA and CHA-OAL in

Luria-Bertani (LB) and Vogel-Bonner (VB) broths: doubling time.

Mean doubling time during exponential growth phase Mutant

LB broth VB broth

CHA-OST 44 mn 68 mn

CHA-ORL 45 mn 55 mn

CHA-OA 81 mn 104 mn

CHA-OAL 88 mn 127 mn

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Figure 1: determination of best time schedule for vaccination using strain CHA-OST. Mice

received the same dose of ovalbumin-delivering CHA-OST with different delay from

tumour implantation (Day 0): at day -14 and -7; at day -7 and 0; at day 0 and day +7; or at

day +7 and +14. A day -14 and day -7 schedule using a CHA-OST strain delivering no

antigen was used as a negative control. Mice were sacrificed when tumour diameter

reached 1 cm.

0

0,25

0,5

0,75

1

surv

ival

0 10 20 30 40 50 60 70time (days)

no antigen D-14 D-7

Ova D+7 D+14

Ova D0 D+7

Ova D-7 D0

Ova D-14 D-7

0

0,25

0,5

0,75

1

surv

ival

0 10 20 30 40 50 60 70time (days)

no antigen D-14 D-7

Ova D+7 D+14

Ova D0 D+7

Ova D-7 D0

Ova D-14 D-7

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Figure 2: in vitro TTSS efficiency of the mutants. A) fluorescence intensity in culture

pellet of wild type (WT) strain and different mutants transformed by plasmid pS54-

GFP_ExsAi with different TTSS-activating conditions. Negative control: CHA-OST

without plasmid. Error bars: one standard error. B) SDS-PAGE analysis of secretion of

S54-Ova by WT strain and different mutants transformed by plasmid pS54-Ova_Exsai.

Culture medium was supplemented with both IPTG and EGTA. Negative control: CHA-

OST without plasmid.

0

10

20

30

40

50

60

70

80

Flu

ore

sce

nce

(a

rbitra

ry u

nits)

CH

A-O

ST

w/o

GF

P

CH

A-W

T

CH

A-O

ST

CH

A-O

RL

CH

A-O

A

CH

A-O

AL

EGTA + IPTGIPTGEGTAno activation

A B

Strain OST WT OST ORL OAL OA

Plasmid none ova ova ova ova ova

Strain: CHA - OST

Plasmid: ova ova ova ova ova

S54-Ova

0

10

20

30

40

50

60

70

80

Flu

ore

sce

nce

(a

rbitra

ry u

nits)

CH

A-O

ST

w/o

GF

P

CH

A-W

T

CH

A-O

ST

CH

A-O

RL

CH

A-O

A

CH

A-O

AL

EGTA + IPTGIPTGEGTAno activation

0

10

20

30

40

50

60

70

80

Flu

ore

sce

nce

(a

rbitra

ry u

nits)

CH

A-O

ST

w/o

GF

P

CH

A-W

T

CH

A-O

ST

CH

A-O

RL

CH

A-O

A

CH

A-O

AL

EGTA + IPTGIPTGEGTAno activation

A B

Strain OST WT OST ORL OAL OA

Plasmid none ova ova ova ova ova

Strain: CHA - OST

Plasmid: ova ova ova ova ova

S54-Ova

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Figure 3: in vivo toxicity (A) and efficiency (B) of TTSS-based mutant vectors. A) mouse

mortality after SC injection of mutants at doses 105, 10

6, 10

7, 10

8 or 10

9. B) survival after

tumour implantation in mice vaccinated beforehand twice by 105 (thick pale grey line), 10

6

(thick dark grey line) or 107 (thick black line) mutant delivering S54-Ova: CHA-OST,

CHA-ORL, CHA-OA, and CHA-OAL. Negative control: 106 CHA-OST not delivering

S54-Ova (thin line).

0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60time (days)

ORL

OA0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60time (days)

OAL0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60

time (days)

0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60time (days)

OST

su

rviv

al

0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60time (days)

ORL

OA0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60time (days)

OAL0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60

time (days)

0

0,2

0,4

0,6

0,8

1

su

rviv

al

0 10 20 30 40 50 60time (days)

OST

su

rviv

al

A B

0/3109

0/3108

0/6107

0/6106

0/6105

CHA-OAL

0/3109

0/3108

0/6107

0/6106

0/6105

CHA-OA

3/3109

3/3108

1/6107

0/6106

0/6105

CHA-ORL

4/6107

0/6106

0/6105

CHA-OST

mortalitydosemutant

0/3109

0/3108

0/6107

0/6106

0/6105

CHA-OAL

0/3109

0/3108

0/6107

0/6106

0/6105

CHA-OA

3/3109

3/3108

1/6107

0/6106

0/6105

CHA-ORL

4/6107

0/6106

0/6105

CHA-OST

mortalitydosemutant

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Table 3: anti-tumour protection after prophylactic vaccination using S54-Ova delivering

CHA-OAL at different schedules and doses: proportion of tumour-free mice at day 45. NC:

negative control (CHA-OST not delivering any antigen).

Total dose Tumour free mice at day 45

NC 2 x 5.106 107 0/5

CHA-OST 2 x 5.106 107 4/6

CHA-OAL 2 x 1.105 2.105 0/6

CHA-OAL 5 x 1.105 5.105 0/6

CHA-OAL 2 x 5.105 106 0/6

CHA-OAL 5 x 2 x 1.105 106 0/6

CHA-OAL 2 x 1.106 2.106 3/5

CHA-OAL 5 x 1.106 5.106 5/6

CHA-OAL 5 x 2 x 1.106 107 5/6

CHA-OAL 2 x 1.107 2.107 5/6

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