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1                                              H. felis antral colonization remained stable over time a
2                                              H. felis can induce a hypertrophic gastropathy in the C5
3                                              H. felis colonization also was increased in Duoxa(+/-) m
4                                              H. felis colonization was significantly greater in the i
5                                              H. felis colonized the mucus layer in the stomachs of Du
6                                              H. felis infection leads to increased apoptosis and alte
7                                              H. felis was inoculated by gastric intubation into SPF C
8                                              H. felis-infected IL-10(-/-) mice may provide a model wi
9 LA2 was observed in BALB/c and C3H/HeJ after H. felis infection, whereas sPLA2 expression was absent
10 ic epithelial pathology even 12 months after H. felis infection.
11 immune-mediated gastric pathology seen after H. felis infection.
12 the protection of the gastric mucosa against H. felis infection.
13 /250 (57%), H. heilmannii in 17/250 (6%) and H. felis in 10/250 (4%), respectively.
14 nduced peritonitis, DSS-induced colitis, and H. felis-induced gastritis.
15                    All the H. heilmannii and H. felis PCR positive patients were also positive for H.
16 uencing of PCR products of H. heilmannii and H. felis was done.
17          The prevalence of H. heilmannii and H. felis was low in our patients with dyspepsia.
18 nd urease B (ureB) gene of H. heilmannii and H. felis.
19 acter bacteria (H. pylori, H. hepaticus, and H. felis) was mediated not by TLR4 but rather by TLR2.
20          The data suggest that H. pylori and H. felis employ conserved mechanisms of ATPase-dependent
21  CT, or both, produced a specific fecal anti-H. felis IgA response, with the highest IgA levels occur
22 ation in the body of the stomach, lower anti-H. felis serum IgG antibody responses (although both the
23 n combination developed increased serum anti-H. felis immunoglobulin G (IgG).
24   Infected animalls developed sustained anti-H. felis serum immunoglobulin G antibody responses.
25 icate substantial antigenic homology between H. felis, H. pylori, and H. bizzozeronii.
26                                         Both H. felis infection and K-ras mutation induced upregulati
27 osis of the antrum and pyloric junction, but H. felis infection of the Apc mutant mouse does not lead
28 yme complex prevents gastric colonization by H. felis and the inflammatory response.
29  In vitro, induction of oxidative defense by H. felis failed to prevent a direct bacteriostatic effec
30   It was concluded that gastritis induced by H. felis is associated with increased HbA(1c) levels in
31                                      Chronic H. felis infection did not alter these proportions, but
32 agnitude between 12 and 15 months of chronic H. felis infection (P = 0.167).
33 AT3-deficient Stat3(SA/SA) mice with chronic H. felis infection, which mimics human H. pylori infecti
34 t other helicobacters (H. canis, H. cineadi, H. felis, H. mustelae, H. nemestrinae, H. pullorum, H. p
35                                 In contrast, H. felis-infected IL-10(-/-) mice develop a severe hyper
36 ion enzymes DdeI and MnlI for distinguishing H. felis from closely related bacteria was examined.
37 undic Pdx1 expression was observed in either H. felis-infected or DMP777-treated mice.
38 r Helicobacter spp. revealed that all except H. felis grew in serum-free, unsupplemented F-12.
39  mice were infected with Helicobacter felis (H. felis) to induce gastritis.
40                     The stomachs of all five H. felis-inoculated cats became colonized, as determined
41                                    Following H. felis challenge, addition of the adjuvant CpG ODN pro
42 ected controls (P = 0.0008 and P = 0.002 for H. felis sonicate and CT, respectively).
43 tis, and four gastric ulcer samples), 10 for H. felis (one gastritis, three duodenal ulcer, and six g
44                                    Blood for H. felis purification was repeatedly collected from sple
45 , mainly CD4(+) for H. pylori and CD8(+) for H. felis.
46                 Sera were also evaluated for H. felis antibody by ELISA.
47  were positive for H. heilmannii and two for H. felis.
48 om the "H. heilmannii"-like organisms (HHLO) H. felis, H. salomonis, and H. bizzozeronii.
49  objective of this study was to determine if H. felis infection alters gastric histopathology, proinf
50 development of gastric atrophy and cancer in H. felis/INS-GAS mice, while the proton pump inhibitor s
51 obacter-associated gastric carcinogenesis in H. felis-infected mice on a uniform C57BL/6 background h
52                                 Gastritis in H. felis-infected CD73-/- mice was significantly worse t
53 xpression of the H2O2-inducible katA gene in H. felis that colonized Duoxa(-/-) mice, compared with t
54 ificant reduction of gastric inflammation in H. felis-infected, as well as immunized/challenged, mice
55 cinogenesis, and novel experiments involving H. felis infection of bone marrow transplanted irradiate
56 ical disease (colitis), and antibody levels (H. felis) were examined.
57               In contrast to wild-type mice, H. felis-infected IL-10(-/-) mice had a marked increase
58 ults indicate that, in the absence of MyD88, H. felis infection enhances the activation of non-canoni
59 tory cytokine expression, or colonization of H. felis was evaluated in CD73-deficient (CD73-/-) mice
60 ally regulate the epithelial consequences of H. felis infection in the stomach, while c-Rel-mediated
61 ght be useful for the serologic diagnosis of H. felis infections in cats.
62 -facilitated diagnosis and discrimination of H. felis infection in cats.
63 ,316-bp DNA fragment of the 16S rRNA gene of H. felis from each of four experimentally infected cats
64 h rUre produces a long-lasting inhibition of H. felis infection but that residual bacteria may produc
65 s and congenic mice with a single isolate of H. felis.
66 treatment did not alter the overall level of H. felis colonization but did result in significant down
67 nd evaluated histologically for magnitude of H. felis infection.
68  PCR assay, the minimum detectable number of H. felis organisms was determined to be between 50 and 7
69 us adjuvant and examined for the presence of H. felis infection and leukocyte infiltration into the g
70  on this sequence data, we designed a set of H. felis-specific primers.
71 9%) than to that of the California strain of H. felis (84%).
72 elated to that of the Ohio-Florida strain of H. felis (89%) than to that of the California strain of
73 were orally infected with a single strain of H. felis, and 2 and 11 weeks after infection, the mice w
74              The sequences of two strains of H. felis from cats in California were identical, as were
75 one of the H. muris strains, four strains of H. felis, and two strains of Eperythrozoon suis were seq
76                        Three were strains of H. felis, one was H. bilis, and one was a novel helicoba
77                            Within 4 weeks of H. felis infection, there are striking alterations in th
78                            Within 4 weeks of H. felis infection, wild-type mice develop a mild, focal
79 id not increase the risk of H. heilmannii or H. felis infection.
80 st similar (97 to 99%) to "H. heilmannii" or H. felis.
81 e H. pylori, an H. pylori cagE(-) mutant, or H. felis were killed 2-24 weeks postchallenge.
82 ion after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any ba
83 pylori and non-Helicobacter pylori organisms H. felis and H. heilmannii and analyzed the association
84 nimals immunized intranasally with sonicated H. felis with CT and CpG.
85 infection with T. gondii alters the specific H. felis immune response, converting a previously resist
86                                     Four SPF H. felis-uninfected cats served as controls.
87                               The suppressed H. felis-induced gastric phenotype of Stat3(SA/SA) mice
88  pronounced gastric atrophy after short-term H. felis colonization with a similar extent of preneopla
89                 These findings indicate that H. felis infection in cats induces lymphoid follicular h
90 n serum from Rag2(-/-) mice, indicating that H. felis activates complement through the classical path
91 cholesterol levels were observed between the H. felis-infected and -uninfected iNOS-/- mice in this s
92 hip of SPEM to the neoplastic process in the H. felis -infected C57BL/6 mouse, we have now studied th
93  corresponding transmembrane segments of the H. felis CopA pump were identified by hydrophobicity ana
94 of E. suis being most similar to that of the H. felis strain from California.
95 dicative of an impaired Th1 component of the H. felis-induced inflammatory response when the influenc
96 ated Helicobacter that is closely related to H. felis, is associated with little or no gastritis, and
97                     T-bet KO mice respond to H. felis infection with a markedly blunted IL-1beta and
98 ficiency and STAT3 activation in response to H. felis infection.
99 rganisms and evaluate the immune response to H. felis.
100 r Th1-associated IgG2c antibody responses to H. felis (P <0.0003); the Th2-associated IgG1 responses
101 gG1), IgG2a, and IgG2c antibody responses to H. felis were determined.
102 ockout mice have increased susceptibility to H. felis-induced gastritis, with enhanced gastric inflam
103 erated development of gastric pathology upon H. felis infection, but the mechanisms leading to this p
104 ucous metaplasia in the fundic mucosa, while H. felis-infected wild-type mice had severe atrophic and
105 pylori and H. heilmannii was 17(6%) and with H. felis was 10(4%), respectively.
106                               Challenge with H. felis increased the inflammatory response in the gast
107 nii and H. pylori and 1(20%) coinfected with H. felis and H. pylori (p = 0.15).
108 nii and H. pylori and 3(60%) coinfected with H. felis and H. pylori (p = 0.66).
109 zyme-linked immunosorbent assay (ELISA) with H. felis ATCC 49179 antigen were performed with 101 seru
110 protection induced by oral immunization with H. felis sonicate and CT.
111 hese proportions, but oral immunization with H. felis sonicate plus cholera toxin (CT) or with CT alo
112 cantly up-regulated in WT mice infected with H. felis (P < 0.05) but were slightly elevated or were a
113 and C57BL/6 (-/-)] were orally infected with H. felis and examined longitudinally using routine histo
114 57BL/6 x 129SvEv)F1] mice were infected with H. felis by oral gavage and were assessed histologically
115 ections from male C57BL/6 mice infected with H. felis for 6 months.
116 nd C57BL/6 wild-type mice were infected with H. felis for either 12 or 18 months.
117 ld-type (WT) C57BL/6 mice were infected with H. felis.
118                               Infection with H. felis induced expression of Duox2 and Duoxa2 in the s
119                One year after infection with H. felis, the wild-type and p53 hemizygous mice showed s
120 in, and the mice were orally inoculated with H. felis.
121 e and for 1 year after oral inoculation with H. felis (ATCC 49179).
122 57BL/6-T-bet knockout (KO) litter mates with H. felis and examined the bacterial colonization, immune
123            Infection of IL-10(-/-) mice with H. felis elicited a severe chronic gastritis and a great
124            Infection of IL-10(-/-) mice with H. felis elicited severe gastritis.
125 r T cell-deficient TCRbetadelta-/- mice with H. felis resulted in high levels of colonization, but no
126 erleukin-10-deficient (IL-10(-/-)) mice with H. felis.

 
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