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1 esis as well as heightened susceptibility to Salmonella infection.
2 ive Salmonella, a phenotype resembling human Salmonella infection.
3 es M cells and SFB levels to protect against Salmonella infection.
4 se can serve as a good animal model to study Salmonella infection.
5 synthesis or modification mainly during the Salmonella infection.
6 ed Ab had little deficiency in resistance to Salmonella infection.
7 role of SIRPalpha for protective immunity to Salmonella infection.
8 ded mice with significant protection against Salmonella infection.
9 ythropoiesis and increased susceptibility to Salmonella infection.
10 ion and systemic inflammation in response to Salmonella infection.
11 lagellin-specific CD4 T cells following oral Salmonella infection.
12 lic abnormalities, or enhanced resistance to Salmonella infection.
13 s and optimal protective immunity to primary Salmonella infection.
14 massive erythropoiesis occurs in response to Salmonella infection.
15 ell death ligand 1) in resistance to primary Salmonella infection.
16 and the resulting susceptibility to enteric Salmonella infection.
17 xacerbates mucosal inflammatory responses to Salmonella infection.
18 demonstrate a global macrophage response to Salmonella infection.
19 hepatobiliary system as the site of chronic Salmonella infection.
20 their host cell targets during each stage of Salmonella infection.
21 showed increased susceptibility to systemic Salmonella infection.
22 es cecal colonization during early stages of Salmonella infection.
23 hese changes conferred greater resistance to Salmonella infection.
24 4 T cells, which are crucial for immunity to Salmonella infection.
25 bably are an underrecognized source of human salmonella infection.
26 innate and adaptive immune responses during Salmonella infection.
27 nt during, and immediately following, active Salmonella infection.
28 neutral sphingolipids did not increase upon Salmonella infection.
29 reversed the deleterious effects of in vivo Salmonella infection.
30 ession in intestinal tissues is increased by Salmonella infection.
31 ation of IL-10 production, and resistance to Salmonella infection.
32 ssion of T-bet is required for resistance to Salmonella infection.
33 inflammation, anemia, and susceptibility to Salmonella infection.
34 role of the chemokine CCL2 in the control of Salmonella infection.
35 dulation on NKT cells in the setting of oral Salmonella infection.
36 age may be important in the establishment of Salmonella infection.
37 d Th17 responses in ex-germ-free mice during Salmonella infection.
38 mice (carrying mutated TLR-4) in response to Salmonella infection.
39 le of IFN-alpha/beta in the host response to Salmonella infection.
40 enotypic response of different cell lines to Salmonella infection.
41 ains of salmonella is rare, as is nosocomial salmonella infection.
42 kout (KO) mice are susceptible profoundly to Salmonella infection.
43 e capacity to protect naive mice from lethal Salmonella infection.
44 ion of IL-18 secretion by macrophages due to Salmonella infection.
45 e expression to the appropriate times during Salmonella infection.
46 recognized by murine T cells responding to a Salmonella infection.
47 or SCF:c-kit interactions in host defense to Salmonella infection.
48 be an important intestinal tract response to Salmonella infection.
49 ogenase LldD in vitro and in mouse models of Salmonella infection.
50 Lsh/Bcg locus and in their susceptibility to Salmonella infection.
51 so dampened the inflammatory response during Salmonella infection.
52 at IL-1beta production is detrimental during Salmonella infection.
53 ain (NICD) and Hes1 were decreased following Salmonella infection.
54 ellular bacterial restriction in the case of Salmonella infection.
55 in nucleation and polymerization defect upon Salmonella infection.
56 targeted for therapy of diarrhoea caused by Salmonella infection.
57 notypic variation in their susceptibility to Salmonella infection.
58 component of the host defense machinery upon Salmonella infection.
59 and functional files, and susceptibility to Salmonella infection.
60 te host defense in homeostasis and following Salmonella infection.
61 anode, which is reversed to the cathode upon Salmonella infection.
62 sible for variation in the susceptibility to Salmonella infection.
63 isease tolerance pathways in endotoxemia and Salmonella infection.
64 ption of raw food as a major risk factor for Salmonella infection.
65 erform lactate fermentation, thus supporting Salmonella infection.
66 onferred crucial protection against systemic Salmonella infection.
67 ntestinal microbial community in response to Salmonella infection.
68 similar to those of wild-type mice following Salmonella infection.
69 ins of the host tryptophan metabolism during Salmonella infection.
70 s new candidates potentially associated with Salmonella infection.
71 -331-3p in regulation of immune responses to Salmonella infection.
72 at may potentially regulate host response to Salmonella infection.
73 ucella but found that it is not required for Salmonella infection.
74 L-17RA expression was generally unchanged in Salmonella infection.
75 way are predisposed to invasive nontyphoidal Salmonella infection.
76 imulation hindered the resolution of primary Salmonella infection.
77 tions and play a crucial role in controlling Salmonella infection.
78 he pathophysiological impact of STAT4 during Salmonella infection.
79 le for cell death associated caspases during Salmonella infection.
80 e to drive robust IL-1beta processing during Salmonella infection.
81 t of inflammatory cells to the spleen during Salmonella infection.
82 duced the adverse effects of H. polygyrus on Salmonella infection.
83 ble phenotype of IFN-gamma-deficient mice to Salmonella infection.
84 e distinct effector functions in response to Salmonella infection.
85 08, we investigated a nationwide outbreak of salmonella infections.
86 l strategies to diagnose, treat, and prevent Salmonella infections.
87 lence in herds is important to prevent human Salmonella infections.
88 contributes to proinflammatory responses to Salmonella infections.
89 previously unrecognized specific features of Salmonella infections.
90 ty enhanced the clearance of multiple-strain Salmonella infections.
91 flammatory cytokines which is typical during Salmonella infections.
92 ating toxin critical for the pathogenesis of Salmonella infections.
93 presenting with fever of unknown origin for Salmonella infections.
94 mediators of resistance to extra-intestinal Salmonella infections.
95 ost cells is crucial for the pathogenesis of Salmonella infections.
96 cellular ATP to confer resistance to enteric Salmonella infections.
97 had significantly higher inflammation after Salmonella infections.
98 nce-associated secreted factor that enhances Salmonella infections.
99 e among the drugs of choice for treatment of Salmonella infections.
100 had significantly higher inflammation after Salmonella infections.
101 of antibacterial strategies to fight against Salmonella infections.
102 ndary protection against otherwise lethal WT Salmonella infections.
103 REI-Bs studied (beach water exposure [OR for Salmonella infection, 28.3 {CI, 7.2-112.2}; OR for Shige
104 ed was associated with a significant risk of salmonella infection (4 of 5 patients had taken fluoroqu
111 regulate a maximal innate immune response to Salmonella infection, allowing a sustained inflammatory
113 lular proliferation within host cells during Salmonella infections, although none have been found to
115 e know quite a bit about the epidemiology of Salmonella infection among domestic fowl, we know little
116 susceptibility to atypical mycobacterial and salmonella infections among individuals whose lymphocyte
117 igate the contribution of IL-18 to resolving Salmonella infections, an attenuated aro-negative mutant
118 Peyer patches are the major entrance of Salmonella infection and antigen transportation in intes
119 lls are activated within a few hours of oral Salmonella infection and are essential for protective im
120 as a susceptibility factor for disseminated Salmonella infection and arginine as a central metabolit
121 We find that Rab32 interacts with IRG1 on Salmonella infection and facilitates the delivery of ita
122 We monitored spleen cell populations during Salmonella infection and found that the most prominent i
124 ntibacterial effect within macrophages after Salmonella infection and to sensitize host cells to Salm
125 re essential for resistance against systemic Salmonella infections and can express the highest protec
126 he pathogenesis of typhoid and non-typhoidal Salmonella infections and demonstrate the utility of hum
128 firms the importance of PMN in resistance to Salmonella infections and shows that this is facilitated
129 etermining the outcome of naturally acquired Salmonella infections and that both vaccine formulation
130 nal surveillance methods for the evidence of Salmonella infections and to determine the extent of out
133 nd intermittent fecal shedding, hallmarks of Salmonella infections, are important for fecal-oral tran
135 e, have attenuated inflammatory responses to Salmonella infection associated with decreased macrophag
136 data show that morphine markedly potentiates Salmonella infection at the gastrointestinal portal of e
139 reography of gene expression is required for Salmonella infection, but basic genetic information such
140 BP-independent manner were more resistant to Salmonella infection, but neutropenic mice were not prot
141 proteins, is critical in such a response to salmonella infection, but the mechanism of how Ipaf is a
142 enia, there was a variable increase in total salmonella infection, but the relative splenic CFU of Sp
143 hoid tissues, their density increases during Salmonella infection, but the underlying molecular mecha
144 a critical cytokine in host defense against salmonella infections, but its role in phagocytic killin
145 stinct microbiota members prevent intestinal Salmonella infection by enhancing antibacterial IFNgamma
146 lagellin in the typhoid-like systemic murine Salmonella infection by measuring bacterial proliferatio
147 n of specific gut bacteria that protect from Salmonella infection by priming host IFN-gamma responses
148 Pase RalA, which we show is triggered during Salmonella infection by the translocated effector, SopE.
149 the role of B cells in acquired immunity to Salmonella infection by using gene-targeted B-cell-defic
150 ast to infection of macrophages by wild-type Salmonella, infection by the sopB deletion mutant had no
151 n the mechanism of DRA downregulation during Salmonella infection, by using murine epithelial enteroi
154 Together, these data suggest that low-dose Salmonella infection can evade flagellin-specific CD4 T
156 pyrin-domain containing protein 3 (NLRP3) by Salmonella infection, CARD9 negatively regulates IL-1bet
158 espond to bacterial and helminth infections: Salmonella infection caused an increase in the abundance
160 d innate IFN-gamma expression in response to Salmonella infection compared with SLC11A1(-) mice, whic
161 vertheless, the initial cellular response to Salmonella infections consists primarily of polymorphonu
165 observed that in primary macrophages, during Salmonella infection, Elmo1 and Med31 specifically affec
166 that bacterial products (LPS), IL-6, RA, and Salmonella infection enhance the expression of the cathe
168 mmune changes and lost resistance to enteric Salmonella infections even in the presence of T. musculi
178 ) are required for robust protection against Salmonella infection; however, the generation of this T
179 eractions in autophagy-dependent response to Salmonella infection, (ii) uncovering gene-environment i
181 testinal disease resulting from nontyphoidal Salmonella infection in an animal with an intact microbi
182 e show that a chronic systemic non-typhoidal Salmonella infection in an immunocompromised human patie
183 of the immune mechanisms protective against Salmonella infection in chickens has not been characteri
185 t cytokine response determine the outcome of Salmonella infection in genetically susceptible and resi
187 nomenon, we examined innate immunity to oral Salmonella infection in Hfe knockout (Hfe(-/-)) mice, a
188 virulence regulators facilitates persistent Salmonella infection in humans, by attenuating Salmonell
189 he innate and adaptive immune systems during Salmonella infection in mice and humans; however, the re
191 roduction and a heightened susceptibility to Salmonella infection in mice undergoing withdrawal from
193 t flocks and eggs at the hatchery in case of Salmonella infection in parent flocks in the Danish poul
199 ure-confirmed Campylobacter and nontyphoidal Salmonella infections in Australia, Canada, and the Unit
201 w of these serovars are responsible for most Salmonella infections in humans and domestic animals.
202 ated with the reported national incidence of Salmonella infections in humans but were correlated with
204 st antimicrobials used for treating invasive Salmonella infections in low- and middle-income countrie
205 t signs of enteritis or enterocolitis due to Salmonella infections in mice has limited the developmen
208 gnized outbreak of fluoroquinolone-resistant salmonella infections in the United States, which occurr
209 outcomes for patients with culture-confirmed Salmonella infection, in 9 states, each of which partici
214 Based upon these findings, we propose that Salmonella infection involves an acid-dependent secretio
217 at an important intestinal tract response to Salmonella infection is an enhanced production of SCF an
220 show that the T cell response to pathogenic Salmonella infection is localized to the gut-associated
225 quinolones, which are used to treat invasive salmonella infections, is rare in the United States.
227 Between 1996 and 2012, 45 outbreaks of human Salmonella infections linked to live poultry from mail-o
228 trogen species (RNS) produced in response to Salmonella infection lock persisters in growth arrest by
230 We found that T cell clonotypes in a mouse Salmonella infection model span early activated CD4(+) T
232 hus, immunologists have frequently turned to Salmonella infection models to expand understanding of h
235 the characteristic inflammatory pathology of Salmonella infection occurs only in PPs and to a lesser
236 0 and the upregulation of this protein after Salmonella infection of eukaryotic cells, this mode of a
239 ngs indicate that camp is not induced during Salmonella infection of MDMs nor is key to Salmonella in
243 ucosal inflammation that is triggered during Salmonella infection of the gastrointestinal and biliary
244 at the SseD protein is required for systemic Salmonella infection of the mouse, and we confirmed the
245 Caspase-3 activation was detected during Salmonella infection of THP-1 cells, but caspase-8 and c
247 his subspecies is responsible for almost all Salmonella infections of mammals and birds, these genes
249 es following infection with Dam(+) or Dam(-) SALMONELLA: Infection of mice with Dam(+) Salmonella res
251 se findings emphasize the profound effect of Salmonella infection on erythroid development and sugges
252 foci within macrophages responding to either Salmonella infection or intoxication by Bacillus anthrac
254 ciprofloxacin remains a common treatment for Salmonella infections, particularly in lower-resource se
258 ples were obtained from patients with recent Salmonella infection, ReA, other SpA, and rheumatoid art
262 in casp-1(-/)- animals appears specific for Salmonella infection since these mice were susceptible t
265 nly partially transferred protection against Salmonella infection, suggesting that minority species w
266 delayed NLRP3 inflammasome activation after Salmonella infection, suggesting that Salmonella may eva
269 -) mice were found to be more susceptible to Salmonella infection than WT mice, as evidenced by high
270 umbers of MDSCs and were more susceptible to Salmonella infection than young mice, suggesting a role
272 ount a multifaceted inflammasome response to Salmonella infection that ultimately restricts intracell
274 he PmrA protein may limit the acute phase of Salmonella infection, thereby enhancing pathogen persist
275 the intestinal host defense against enteric Salmonella infections through Asc- and Il1r1-dependent T
277 extra- to intracellular environments during Salmonella infection triggers changes in Ag expression t
278 onitis, hepatic ischemia-reperfusion injury, Salmonella infection, uveitis and Sjogren's syndrome, PE
280 showed that this miRNA specifically inhibits Salmonella infection via modulation of endolysosomal tra
281 Here, using a mouse model of persistent Salmonella infection, we identify a host-protective role
282 yroptosis, necroptosis, and apoptosis during Salmonella infection, we infected mice and macrophages d
283 e the extent to which macrophages respond to Salmonella infection, we infected RAW 264.7 macrophages
285 In order to identify key players involved in Salmonella infection, we performed a global host phospho
286 ts with antimicrobial-resistant nontyphoidal Salmonella infection were more likely to have bloodstrea
287 rugs that are not appropriate for therapy of Salmonella infections were tested and reported by 136 (9
288 RAW264.7 macrophages are more responsive to Salmonella infection when treated with thapsigargin but
289 g human-relevant differences in nontyphoidal Salmonella infections, whereas differentiated human THP-
290 tilized both the traditional model of murine Salmonella infection, wherein low-dose oral infection of
291 t PedsCom mice retain high susceptibility to Salmonella infection, which is characteristic of young m
292 bility of CD4(+) T cells during a persistent Salmonella infection, which is typical of persistent pha
293 ntaining vacuoles and host mitochondria upon Salmonella infection, which was significantly impaired i
294 ved understanding of the biology of invasive Salmonella infection will facilitate the development of
295 m mathematical models of in vivo dynamics of Salmonella infections with experimental observation of b
297 lium and lamina propria up to 2 months after Salmonella infection, with an abundant presence of macro
298 ical consequences of NO production following Salmonella infection, with NO being necessary for host d
300 are essential mediators of immunity against Salmonella infection, yet it is not clear whether target