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1 xacerbates mucosal inflammatory responses to Salmonella infection.
2 demonstrate a global macrophage response to Salmonella infection.
3 their host cell targets during each stage of Salmonella infection.
4 showed increased susceptibility to systemic Salmonella infection.
5 es cecal colonization during early stages of Salmonella infection.
6 hese changes conferred greater resistance to Salmonella infection.
7 bably are an underrecognized source of human salmonella infection.
8 innate and adaptive immune responses during Salmonella infection.
9 nt during, and immediately following, active Salmonella infection.
10 neutral sphingolipids did not increase upon Salmonella infection.
11 reversed the deleterious effects of in vivo Salmonella infection.
12 ession in intestinal tissues is increased by Salmonella infection.
13 ation of IL-10 production, and resistance to Salmonella infection.
14 ssion of T-bet is required for resistance to Salmonella infection.
15 role of the chemokine CCL2 in the control of Salmonella infection.
16 similar to those of wild-type mice following Salmonella infection.
17 dulation on NKT cells in the setting of oral Salmonella infection.
18 age may be important in the establishment of Salmonella infection.
19 mice (carrying mutated TLR-4) in response to Salmonella infection.
20 ins of the host tryptophan metabolism during Salmonella infection.
21 le of IFN-alpha/beta in the host response to Salmonella infection.
22 ains of salmonella is rare, as is nosocomial salmonella infection.
23 kout (KO) mice are susceptible profoundly to Salmonella infection.
24 e capacity to protect naive mice from lethal Salmonella infection.
25 ion of IL-18 secretion by macrophages due to Salmonella infection.
26 e expression to the appropriate times during Salmonella infection.
27 s new candidates potentially associated with Salmonella infection.
28 recognized by murine T cells responding to a Salmonella infection.
29 or SCF:c-kit interactions in host defense to Salmonella infection.
30 be an important intestinal tract response to Salmonella infection.
31 Lsh/Bcg locus and in their susceptibility to Salmonella infection.
32 -331-3p in regulation of immune responses to Salmonella infection.
33 at may potentially regulate host response to Salmonella infection.
34 ucella but found that it is not required for Salmonella infection.
35 L-17RA expression was generally unchanged in Salmonella infection.
36 way are predisposed to invasive nontyphoidal Salmonella infection.
37 imulation hindered the resolution of primary Salmonella infection.
38 tions and play a crucial role in controlling Salmonella infection.
39 ption of raw food as a major risk factor for Salmonella infection.
40 he pathophysiological impact of STAT4 during Salmonella infection.
41 e to drive robust IL-1beta processing during Salmonella infection.
42 t of inflammatory cells to the spleen during Salmonella infection.
43 duced the adverse effects of H. polygyrus on Salmonella infection.
44 erform lactate fermentation, thus supporting Salmonella infection.
45 ble phenotype of IFN-gamma-deficient mice to Salmonella infection.
46 e distinct effector functions in response to Salmonella infection.
47 esis as well as heightened susceptibility to Salmonella infection.
48 ive Salmonella, a phenotype resembling human Salmonella infection.
49 se can serve as a good animal model to study Salmonella infection.
50 synthesis or modification mainly during the Salmonella infection.
51 ed Ab had little deficiency in resistance to Salmonella infection.
52 role of SIRPalpha for protective immunity to Salmonella infection.
53 ded mice with significant protection against Salmonella infection.
54 ythropoiesis and increased susceptibility to Salmonella infection.
55 ion and systemic inflammation in response to Salmonella infection.
56 lagellin-specific CD4 T cells following oral Salmonella infection.
57 lic abnormalities, or enhanced resistance to Salmonella infection.
58 s and optimal protective immunity to primary Salmonella infection.
59 onferred crucial protection against systemic Salmonella infection.
60 massive erythropoiesis occurs in response to Salmonella infection.
61 ell death ligand 1) in resistance to primary Salmonella infection.
62 and the resulting susceptibility to enteric Salmonella infection.
63 lence in herds is important to prevent human Salmonella infections.
64 contributes to proinflammatory responses to Salmonella infections.
65 previously unrecognized specific features of Salmonella infections.
66 ty enhanced the clearance of multiple-strain Salmonella infections.
67 flammatory cytokines which is typical during Salmonella infections.
68 ating toxin critical for the pathogenesis of Salmonella infections.
69 mediators of resistance to extra-intestinal Salmonella infections.
70 ost cells is crucial for the pathogenesis of Salmonella infections.
71 e among the drugs of choice for treatment of Salmonella infections.
72 of antibacterial strategies to fight against Salmonella infections.
73 ndary protection against otherwise lethal WT Salmonella infections.
74 08, we investigated a nationwide outbreak of salmonella infections.
75 l strategies to diagnose, treat, and prevent Salmonella infections.
76 REI-Bs studied (beach water exposure [OR for Salmonella infection, 28.3 {CI, 7.2-112.2}; OR for Shige
77 ed was associated with a significant risk of salmonella infection (4 of 5 patients had taken fluoroqu
82 regulate a maximal innate immune response to Salmonella infection, allowing a sustained inflammatory
83 lular proliferation within host cells during Salmonella infections, although none have been found to
84 e know quite a bit about the epidemiology of Salmonella infection among domestic fowl, we know little
85 susceptibility to atypical mycobacterial and salmonella infections among individuals whose lymphocyte
86 igate the contribution of IL-18 to resolving Salmonella infections, an attenuated aro-negative mutant
88 lls are activated within a few hours of oral Salmonella infection and are essential for protective im
89 We monitored spleen cell populations during Salmonella infection and found that the most prominent i
91 ntibacterial effect within macrophages after Salmonella infection and to sensitize host cells to Salm
92 firms the importance of PMN in resistance to Salmonella infections and shows that this is facilitated
93 etermining the outcome of naturally acquired Salmonella infections and that both vaccine formulation
97 e, have attenuated inflammatory responses to Salmonella infection associated with decreased macrophag
98 data show that morphine markedly potentiates Salmonella infection at the gastrointestinal portal of e
100 reography of gene expression is required for Salmonella infection, but basic genetic information such
101 BP-independent manner were more resistant to Salmonella infection, but neutropenic mice were not prot
102 proteins, is critical in such a response to salmonella infection, but the mechanism of how Ipaf is a
103 enia, there was a variable increase in total salmonella infection, but the relative splenic CFU of Sp
104 hoid tissues, their density increases during Salmonella infection, but the underlying molecular mecha
105 a critical cytokine in host defense against salmonella infections, but its role in phagocytic killin
106 stinct microbiota members prevent intestinal Salmonella infection by enhancing antibacterial IFNgamma
107 lagellin in the typhoid-like systemic murine Salmonella infection by measuring bacterial proliferatio
108 n of specific gut bacteria that protect from Salmonella infection by priming host IFN-gamma responses
109 Pase RalA, which we show is triggered during Salmonella infection by the translocated effector, SopE.
110 the role of B cells in acquired immunity to Salmonella infection by using gene-targeted B-cell-defic
111 ast to infection of macrophages by wild-type Salmonella, infection by the sopB deletion mutant had no
113 Together, these data suggest that low-dose Salmonella infection can evade flagellin-specific CD4 T
115 pyrin-domain containing protein 3 (NLRP3) by Salmonella infection, CARD9 negatively regulates IL-1bet
116 espond to bacterial and helminth infections: Salmonella infection caused an increase in the abundance
118 d innate IFN-gamma expression in response to Salmonella infection compared with SLC11A1(-) mice, whic
119 vertheless, the initial cellular response to Salmonella infections consists primarily of polymorphonu
123 observed that in primary macrophages, during Salmonella infection, Elmo1 and Med31 specifically affec
124 that bacterial products (LPS), IL-6, RA, and Salmonella infection enhance the expression of the cathe
133 eractions in autophagy-dependent response to Salmonella infection, (ii) uncovering gene-environment i
135 testinal disease resulting from nontyphoidal Salmonella infection in an animal with an intact microbi
136 e show that a chronic systemic non-typhoidal Salmonella infection in an immunocompromised human patie
137 of the immune mechanisms protective against Salmonella infection in chickens has not been characteri
139 t cytokine response determine the outcome of Salmonella infection in genetically susceptible and resi
140 nomenon, we examined innate immunity to oral Salmonella infection in Hfe knockout (Hfe(-/-)) mice, a
141 he innate and adaptive immune systems during Salmonella infection in mice and humans; however, the re
143 roduction and a heightened susceptibility to Salmonella infection in mice undergoing withdrawal from
151 w of these serovars are responsible for most Salmonella infections in humans and domestic animals.
152 ated with the reported national incidence of Salmonella infections in humans but were correlated with
153 t signs of enteritis or enterocolitis due to Salmonella infections in mice has limited the developmen
156 gnized outbreak of fluoroquinolone-resistant salmonella infections in the United States, which occurr
157 outcomes for patients with culture-confirmed Salmonella infection, in 9 states, each of which partici
162 Based upon these findings, we propose that Salmonella infection involves an acid-dependent secretio
164 at an important intestinal tract response to Salmonella infection is an enhanced production of SCF an
167 show that the T cell response to pathogenic Salmonella infection is localized to the gut-associated
172 quinolones, which are used to treat invasive salmonella infections, is rare in the United States.
174 Between 1996 and 2012, 45 outbreaks of human Salmonella infections linked to live poultry from mail-o
175 We found that T cell clonotypes in a mouse Salmonella infection model span early activated CD4(+) T
176 hus, immunologists have frequently turned to Salmonella infection models to expand understanding of h
178 the characteristic inflammatory pathology of Salmonella infection occurs only in PPs and to a lesser
179 0 and the upregulation of this protein after Salmonella infection of eukaryotic cells, this mode of a
182 ngs indicate that camp is not induced during Salmonella infection of MDMs nor is key to Salmonella in
185 ucosal inflammation that is triggered during Salmonella infection of the gastrointestinal and biliary
186 at the SseD protein is required for systemic Salmonella infection of the mouse, and we confirmed the
187 Caspase-3 activation was detected during Salmonella infection of THP-1 cells, but caspase-8 and c
188 his subspecies is responsible for almost all Salmonella infections of mammals and birds, these genes
190 es following infection with Dam(+) or Dam(-) SALMONELLA: Infection of mice with Dam(+) Salmonella res
192 se findings emphasize the profound effect of Salmonella infection on erythroid development and sugges
193 foci within macrophages responding to either Salmonella infection or intoxication by Bacillus anthrac
197 ples were obtained from patients with recent Salmonella infection, ReA, other SpA, and rheumatoid art
199 in casp-1(-/)- animals appears specific for Salmonella infection since these mice were susceptible t
202 delayed NLRP3 inflammasome activation after Salmonella infection, suggesting that Salmonella may eva
205 -) mice were found to be more susceptible to Salmonella infection than WT mice, as evidenced by high
206 umbers of MDSCs and were more susceptible to Salmonella infection than young mice, suggesting a role
208 he PmrA protein may limit the acute phase of Salmonella infection, thereby enhancing pathogen persist
210 extra- to intracellular environments during Salmonella infection triggers changes in Ag expression t
211 onitis, hepatic ischemia-reperfusion injury, Salmonella infection, uveitis and Sjogren's syndrome, PE
213 e the extent to which macrophages respond to Salmonella infection, we infected RAW 264.7 macrophages
215 ts with antimicrobial-resistant nontyphoidal Salmonella infection were more likely to have bloodstrea
216 rugs that are not appropriate for therapy of Salmonella infections were tested and reported by 136 (9
217 tilized both the traditional model of murine Salmonella infection, wherein low-dose oral infection of
218 bility of CD4(+) T cells during a persistent Salmonella infection, which is typical of persistent pha
219 ved understanding of the biology of invasive Salmonella infection will facilitate the development of
220 m mathematical models of in vivo dynamics of Salmonella infections with experimental observation of b
222 lium and lamina propria up to 2 months after Salmonella infection, with an abundant presence of macro
223 ical consequences of NO production following Salmonella infection, with NO being necessary for host d
225 are essential mediators of immunity against Salmonella infection, yet it is not clear whether target
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