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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 t other helicobacters (H. canis, H. cineadi, H. felis, H. mustelae, H. nemestrinae, H. pullorum, H. p
34                                 In contrast, H. felis-infected IL-10(-/-) mice develop a severe hyper
35 ion enzymes DdeI and MnlI for distinguishing H. felis from closely related bacteria was examined.
36 undic Pdx1 expression was observed in either H. felis-infected or DMP777-treated mice.
37 r Helicobacter spp. revealed that all except H. felis grew in serum-free, unsupplemented F-12.
38  mice were infected with Helicobacter felis (H. felis) to induce gastritis.
39                     The stomachs of all five H. felis-inoculated cats became colonized, as determined
40                                    Following H. felis challenge, addition of the adjuvant CpG ODN pro
41 ected controls (P = 0.0008 and P = 0.002 for H. felis sonicate and CT, respectively).
42                                    Blood for H. felis purification was repeatedly collected from sple
43 , mainly CD4(+) for H. pylori and CD8(+) for H. felis.
44                 Sera were also evaluated for H. felis antibody by ELISA.
45  were positive for H. heilmannii and two for H. felis.
46 om the "H. heilmannii"-like organisms (HHLO) H. felis, H. salomonis, and H. bizzozeronii.
47  objective of this study was to determine if H. felis infection alters gastric histopathology, proinf
48 development of gastric atrophy and cancer in H. felis/INS-GAS mice, while the proton pump inhibitor s
49 obacter-associated gastric carcinogenesis in H. felis-infected mice on a uniform C57BL/6 background h
50                                 Gastritis in H. felis-infected CD73-/- mice was significantly worse t
51 xpression of the H2O2-inducible katA gene in H. felis that colonized Duoxa(-/-) mice, compared with t
52 ificant reduction of gastric inflammation in H. felis-infected, as well as immunized/challenged, mice
53 cinogenesis, and novel experiments involving H. felis infection of bone marrow transplanted irradiate
54 ical disease (colitis), and antibody levels (H. felis) were examined.
55               In contrast to wild-type mice, H. felis-infected IL-10(-/-) mice had a marked increase
56 tory cytokine expression, or colonization of H. felis was evaluated in CD73-deficient (CD73-/-) mice
57 ally regulate the epithelial consequences of H. felis infection in the stomach, while c-Rel-mediated
58 ght be useful for the serologic diagnosis of H. felis infections in cats.
59 -facilitated diagnosis and discrimination of H. felis infection in cats.
60 ,316-bp DNA fragment of the 16S rRNA gene of H. felis from each of four experimentally infected cats
61 h rUre produces a long-lasting inhibition of H. felis infection but that residual bacteria may produc
62 s and congenic mice with a single isolate of H. felis.
63 treatment did not alter the overall level of H. felis colonization but did result in significant down
64 nd evaluated histologically for magnitude of H. felis infection.
65  PCR assay, the minimum detectable number of H. felis organisms was determined to be between 50 and 7
66 us adjuvant and examined for the presence of H. felis infection and leukocyte infiltration into the g
67  on this sequence data, we designed a set of H. felis-specific primers.
68 9%) than to that of the California strain of H. felis (84%).
69 elated to that of the Ohio-Florida strain of H. felis (89%) than to that of the California strain of
70 were orally infected with a single strain of H. felis, and 2 and 11 weeks after infection, the mice w
71              The sequences of two strains of H. felis from cats in California were identical, as were
72 one of the H. muris strains, four strains of H. felis, and two strains of Eperythrozoon suis were seq
73                        Three were strains of H. felis, one was H. bilis, and one was a novel helicoba
74                            Within 4 weeks of H. felis infection, there are striking alterations in th
75                            Within 4 weeks of H. felis infection, wild-type mice develop a mild, focal
76 id not increase the risk of H. heilmannii or H. felis infection.
77 st similar (97 to 99%) to "H. heilmannii" or H. felis.
78 e H. pylori, an H. pylori cagE(-) mutant, or H. felis were killed 2-24 weeks postchallenge.
79 ion after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any ba
80 pylori and non-Helicobacter pylori organisms H. felis and H. heilmannii and analyzed the association
81 nimals immunized intranasally with sonicated H. felis with CT and CpG.
82 infection with T. gondii alters the specific H. felis immune response, converting a previously resist
83                                     Four SPF H. felis-uninfected cats served as controls.
84  pronounced gastric atrophy after short-term H. felis colonization with a similar extent of preneopla
85                 These findings indicate that H. felis infection in cats induces lymphoid follicular h
86 n serum from Rag2(-/-) mice, indicating that H. felis activates complement through the classical path
87 cholesterol levels were observed between the H. felis-infected and -uninfected iNOS-/- mice in this s
88 hip of SPEM to the neoplastic process in the H. felis -infected C57BL/6 mouse, we have now studied th
89  corresponding transmembrane segments of the H. felis CopA pump were identified by hydrophobicity ana
90 of E. suis being most similar to that of the H. felis strain from California.
91 dicative of an impaired Th1 component of the H. felis-induced inflammatory response when the influenc
92 ated Helicobacter that is closely related to H. felis, is associated with little or no gastritis, and
93                     T-bet KO mice respond to H. felis infection with a markedly blunted IL-1beta and
94 rganisms and evaluate the immune response to H. felis.
95 r Th1-associated IgG2c antibody responses to H. felis (P <0.0003); the Th2-associated IgG1 responses
96 gG1), IgG2a, and IgG2c antibody responses to H. felis were determined.
97 ockout mice have increased susceptibility to H. felis-induced gastritis, with enhanced gastric inflam
98 ucous metaplasia in the fundic mucosa, while H. felis-infected wild-type mice had severe atrophic and
99 pylori and H. heilmannii was 17(6%) and with H. felis was 10(4%), respectively.
100                               Challenge with H. felis increased the inflammatory response in the gast
101 nii and H. pylori and 1(20%) coinfected with H. felis and H. pylori (p = 0.15).
102 nii and H. pylori and 3(60%) coinfected with H. felis and H. pylori (p = 0.66).
103 zyme-linked immunosorbent assay (ELISA) with H. felis ATCC 49179 antigen were performed with 101 seru
104 protection induced by oral immunization with H. felis sonicate and CT.
105 hese proportions, but oral immunization with H. felis sonicate plus cholera toxin (CT) or with CT alo
106 cantly up-regulated in WT mice infected with H. felis (P < 0.05) but were slightly elevated or were a
107 and C57BL/6 (-/-)] were orally infected with H. felis and examined longitudinally using routine histo
108 57BL/6 x 129SvEv)F1] mice were infected with H. felis by oral gavage and were assessed histologically
109 ections from male C57BL/6 mice infected with H. felis for 6 months.
110 nd C57BL/6 wild-type mice were infected with H. felis for either 12 or 18 months.
111 ld-type (WT) C57BL/6 mice were infected with H. felis.
112                               Infection with H. felis induced expression of Duox2 and Duoxa2 in the s
113                One year after infection with H. felis, the wild-type and p53 hemizygous mice showed s
114 in, and the mice were orally inoculated with H. felis.
115 e and for 1 year after oral inoculation with H. felis (ATCC 49179).
116 57BL/6-T-bet knockout (KO) litter mates with H. felis and examined the bacterial colonization, immune
117            Infection of IL-10(-/-) mice with H. felis elicited a severe chronic gastritis and a great
118            Infection of IL-10(-/-) mice with H. felis elicited severe gastritis.
119 r T cell-deficient TCRbetadelta-/- mice with H. felis resulted in high levels of colonization, but no
120 erleukin-10-deficient (IL-10(-/-)) mice with H. felis.

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