Our study indicates that colonic epithelial cells may respond to an inflammatory milieu by inducing myofibroblast functions similar to those observed during intestinal fibrosis.

Post-inflammatory scarring is the end-result of excessive extracellular matrix (ECM) accumulation and tissue architectural destruction. It represents a failure to effectively remodel ECM and achieve proper reinstitution and healing during chronic relapsing inflammatory processes. Scarring may affect the functionality of any organ, and in the case of inflammatory bowel disease (IBD)-associated fibrosis leads to stricture formation and often surgery to remove the affected bowel. The activated myofibroblast is the final effector cell that overproduces ECM under the influence of various mediators generated by an intense interplay of classic and non-classic immune cells. This review focuses on how proinflammatory mediators from various sources produced in different stages of intestinal inflammation can form profibrotic pathways that eventually lead to tissue scarring through sustained activation of myofibroblasts.

In about half of patients with unilateral varicosities, CVD developed in the contralateral initially asymptomatic limb in 5 years. CVD progression consisted of reflux development and clinical deterioration of the affected limbs. Obesity, orthostatism, and noncompliance with ESU were independent risk factors for CVD progression, but ET and multiparity were not. Maintenance of a normal body weight, limitation of prolonged orthostatism, and systematic ESU may be recommended in patients with CVD to limit future disease progression.

SummaryHuman colonic epithelial cells express T helper type 1 (Th1)-associated chemoattractants, yet little is known about the production of Th2-associated chemoattractants. CCL11/eotaxin-1, CCL24/eotaxin-2 and CCL26/eotaxin-3 are known to attract CCR3-expressing, Th2-polarized lymphocytes. We studied constitutive and inflammation-induced expression and production of CCR3 together with its ligands in the colon and peripheral blood of patients with inflammatory bowel disease (IBD) by flow cytometry, reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). We further defined the regulated expression of these chemokines by RT-PCR and ELISA using cultured human epithelial cell lines. A higher fraction of peripheral T lymphocytes were found to be positive for CCR3 in patients with ulcerative colitis (UC) compared to Crohn's disease (CD), while almost no CCR3 + T cells were found in normal controls (NC). Similarly, higher and more frequent expression of CCR3 was observed in colonic biopsies from patients with UC, regardless of the disease activity, when compared to CD or NCs. Serum CCL11/eotaxin-1 was increased significantly in UC (306 Ϯ 87 pg/ml) and less so in CD (257 Ϯ 43 pg/ml), whereas CCL24/eotaxin-2, and CCL26/eotaxin-3 were increased only in UC. Colonic expression of the three chemokines was minimal in NCs but high in inflammatory bowel diseases (especially UC) and was independent of disease activity. Th2, and to a lesser extent Th1, cytokines were able to induce expression and production of all three eotaxins from colonic epithelial cells in culture. CCR3 and ligands over-expression would appear to be a characteristic of UC. The production of CCR3 ligands by human colonic epithelial cells suggests further that epithelium can play a role in modulating pathological T cell-mediated mucosal inflammation.

An 87-year-old man was admitted to hospital because of fever, productive cough, dyspnea and altered consciousness. His medical history was significant for chronic obstructive pulmonary disease. He owned several pets. Physical examination and a chest radiograph revealed right upper lobe pneumonia. Blood cultures taken on admission yielded Pasteurella multocida and antimicrobial susceptibility testing showed susceptibility to beta-lactams. The fever subsided four days after treatment with intravenous ceftriaxone and the patient was discharged in a very good clinical condition after two weeks of treatment. Although no history of bites or scratches was documented, it is likely that our patient was exposed to the secretions of his many pets through inhalation of contaminated aerosols. This resulted in tracheobronchial tree colonization by P. multocida, which later developed into pneumonia. Close animal contact should be avoided by frail, elderly patients with chronic pulmonary diseases, as it is a risk factor for pneumonia due to Pasteurella spp.

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Our results suggest that cSEMFs have a central role in inflammation and fibrosis, as they express a great variety of Th-related cytokine receptors, making them responsive to pro-inflammatory cytokines, abundant in the inflamed mucosa of CD patients.

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