Acute colitis caused by Campylobacter fetus ss. jejuni

Blaser, Martin J.; Parsons, Robert B.; Wang, Wen-Lan Lou

doi:10.1016/0016-5085(80)90855-0

Cited by 116 publications

(28 citation statements)

References 27 publications

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“…Since neutrophil infiltration and crypt abscesses are hallmarks of campylobacteriosis in both human and in the Il10 −/− murine model (13, 15), we speculated that signal-induced neutrophil recruitment/activation would be important in host pathogenesis. Among PI3K family members, the class I B PI3Kγ has been implicated in leukocyte migration and activation.…”

Section: Resultsmentioning

confidence: 99%

“…We and others have recently showed that Il10 −/− mice represent a powerful model to study colonization, infection, bacterial translocation and inflammatory responses (12–14). Moreover, a recent study showed that the colon of C. jejuni infected Il10 −/− mice showed increased expression of the chemoattractant Cxcl2 which correlates with the formation of numerous crypt abscesses and neutrophil infiltration, a phenotype commonly observed in human campylobacteriosis (13, 15). Similarly, CXCL-2 mediates neutrophil recruitment into intestinal payer’s patches (PP) and MLN in Salmonella -infected mice (16), therefore this chemokine may play an important role in campylobacteriosis.…”

Section: Introductionmentioning

confidence: 99%

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Phosphatidylinositol 3-Kinase-γ Signaling Promotes Campylobacter jejuni–Induced Colitis through Neutrophil Recruitment in Mice

Sun

Liu

Sartor

et al. 2013

The Journal of Immunology

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Crypt abscesses caused by excessive neutrophil accumulation are prominent features of human campylobacteriosis and its associated pathology. The molecular and cellular events responsible for this pathological situation are currently unknown. We investigated the contribution of PI3Kγ signaling in Campylobacter jejuni-induced neutrophil accumulation and intestinal inflammation. Germ-free and specific pathogen free Il10−/−and germ-free Il10−/−; Rag2−/− mice were infected with C. jejuni (109 CFU/mouse). PI3Kγ signaling was manipulated using either the pharmacological PI3Kγ inhibitor AS252424 (i.p. 10 mg/kg daily) or genetically using Pi3γ−/− mice. After up to 14 days, inflammation was assessed histologically and by measuring levels of colonic Il1β, Cxcl2 and Il17a mRNA. Neutrophils were depleted using anti-Gr1 antibody (i.p. 0.5 mg/mouse/every 3 days). Using germ-free Il10−/−; Rag2−/− mice, we observed that innate immune cells are the main cellular compartment responsible for campylobacteriosis. Pharmacological blockade of PI3Kγ signaling diminished C. jejuni-induced intestinal inflammation, neutrophil accumulation and NF-κB activity, which correlated with reduced Il1β (77%), Cxcl2 (73%) and Il17a (72%) mRNA accumulation. Moreover, Pi3kγ−/− mice pretreated with anti-IL-10R were resistant to C. jejuni-induced intestinal inflammation compared to Wt mice. This improvement was accompanied by a reduction of C. jejuni translocation into the colon and extra-intestinal tissues and by attenuation of neutrophil migratory capacity. Furthermore, neutrophil depletion attenuated C. jejuni-induced crypt abscesses and intestinal inflammation. Our findings indicate that C. jejuni-induced PI3Kγ signaling mediates neutrophil recruitment and intestinal inflammation in Il10−/− mice. Selective pharmacological inhibition of PI3Kγ may represent a novel means to alleviate severe cases of campylobacteriosis, especially in antibiotic-resistant strains.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Phosphatidylinositol 3-Kinase-γ Signaling Promotes Campylobacter jejuni–Induced Colitis through Neutrophil Recruitment in Mice

Sun

Liu

Sartor

et al. 2013

The Journal of Immunology

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“…It sometimes runs a more protracted course with fever, backache, myalgias, and abdominal pain, which occasionally is severe enough to mimic an acute abdomen. Occasionally an acute hemorrhagic colitis is seen with clinical presentation, endoscopic appearance, and histopathology indistinguishable from acute UC (91)(92)(93)(94)(95). Segmental colitis may also be seen (96).…”

Section: Campylobacter Jejunimentioning

confidence: 99%

Clinical evaluation and management of acute severe colitis

Blomberg

2007

Inflamm Bowel Dis

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“…The jejunum and ileum have been regarded as primary sites of infection, but in recent studies the colon is mentioned as an important site of involvement [4,8,11]. The incubation period is probably 3-5 days, sometimes longer.…”

Section: Discussionmentioning

confidence: 99%

“…The endoscopic findings are grossly described as inflamed mucosa with edema, bloody exudate, granularity, friability and sometimes fine ulcerations [4,5,8]. Because the changes can regress quickly, the correlation between roentgenologic and endoscopic findings is difficult or impossible to make when the interval between the 2 examinations is too long.…”

Section: Discussionmentioning

confidence: 99%

Roentgenologic changes of the colon inCampylobacter infection

Tielbeek

Rosenbusch

Muytjens

et al. 1985

Gastrointest Radiol

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A double-contrast examination of the colon was performed during diarrheal illness in 5 patients with Campylobacter infection. The findings in these 5 patients were aphthoid ulcers and stippled appearance. In 1 patient with stool culture positive for Campylobacter, double-contrast study of the colon 9 days later showed no abnormalities. In a 12-year-old boy lymphoid hyperplasia could be observed as well as the aphthoid ulcers. All the abnormalities were segmental, more often localized in the rectosigmoid. No changes were found in the ascending colon. Histopathologic studies of the biopsy specimens taken endoscopically in 3 patients showed a nonspecific inflammatory reaction.

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Acute colitis caused by Campylobacter fetus ss. jejuni

Cited by 116 publications

References 27 publications

Phosphatidylinositol 3-Kinase-γ Signaling Promotes Campylobacter jejuni–Induced Colitis through Neutrophil Recruitment in Mice

Phosphatidylinositol 3-Kinase-γ Signaling Promotes Campylobacter jejuni–Induced Colitis through Neutrophil Recruitment in Mice

Clinical evaluation and management of acute severe colitis

Roentgenologic changes of the colon inCampylobacter infection

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