Chronic Colitis Due to Leishmania Infection in Two Dogs

Ferrer, L.; B, Juanola; Ramos, Jonathan Hernández; Ramis, Antonio

doi:10.1177/030098589102800414

Cited by 53 publications

(59 citation statements)

References 5 publications

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“…However, Th2 cells have been shown to exacerbate colitis (14), and both Th1 and Th2 cells could adoptively transfer colitis in SCID mice in an Ag-specific (15) and a nonspecific manner (11). It has also been reported that colitis could be accelerated by Leishmania infection in dogs (16), but the mechanism involved remains unknown. Our data demonstrated that cutaneous Leishmania infection markedly exacerbated the colitis induced by CD4 ϩ CD25 Ϫ T cells in SCID mice, with increased disease incidence (from 50 to 100%) and severity (clinical score from 1 to 3/4).…”

Section: Discussionmentioning

confidence: 99%

CD4+CD25+ Regulatory T Cells Cure Murine Colitis: The Role of IL-10, TGF-β, and CTLA4

Liu

et al. 2003

The Journal of Immunology

274

230

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Regulatory T cells are critical in regulating the immune response, and therefore play an important role in the defense against infection and control of autoimmune diseases. However, a therapeutic role of regulatory T cells in an established disease has not been fully established. In this study, we provide direct evidence that CD4+CD25+ regulatory T cells can cure an established, severe, and progressive colitis. SCID mice developed severe colitis when adoptively transferred with naive CD4+CD25− T cells and infected with the protozoan parasite Leishmania major. The disease development can be completely halted and symptoms reversed, with a healthy outcome, by transferring freshly isolated or activated CD4+CD25+ T cells from syngeneic donors. The therapeutic effect of the regulatory T cells was completely blocked by treatment of the recipients with anti-IL-10R, anti-CTLA4, or anti-TGF-β Ab. However, the resurgence of colitis under these treatments was not accompanied by the reactivation of Th1 or Th2 response nor was it correlated to the parasite load. These results therefore demonstrate that CD4+CD25+ T cells are therapeutic and that the effect is mediated by both IL-10/TGF-β-dependent and independent mechanisms. Furthermore, colitis can manifest independent of Th1 and Th2 responses.

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Section: Discussionmentioning

confidence: 99%

CD4+CD25+ Regulatory T Cells Cure Murine Colitis: The Role of IL-10, TGF-β, and CTLA4

Liu

et al. 2003

The Journal of Immunology

274

230

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“…3 This observation, taken with the positive correlation between colonic parasitism and colonoscopic gross pathology also noticed in the same study, may justify the differentiation of CanL colitis from the idiopathic, food-induced, and parasitic disease. 46 Finally, in a recent study where the whole gastrointestinal tract of asymptomatic and symptomatic leishmanial dogs was examined histologically, the typical, though mild, lesions of the disease were demonstrated all over its length, along with a high parasitic load, which was more intense in the colon, regardless of clinical status. 114 The relationship between cardiopulmonary disease and L. infantum is rather unclear with its pathological conditions-notably, nonsuppurative myocarditis, fibrinous pericarditis, and pneumonia-being a rare occurrence.…”

Section: General Pathomechanismsmentioning

confidence: 99%

“…49,75,108,149 Digestive disease in CanL is an uncommon to rare cause to admit leishmanial dogs and is mainly expressed as chronic hepatitis or chronic colitis, the subclinical form of which far outnumbers the clinical one. 3,46,120 In the liver, chronic granulomatous inflammation may involve the sinusoids, portal area, or capsule or become diffuse along with the presence of parasites that may also be seen within Kupffer cells and hepatocytes. 43,120 Hepatomegaly, which is far more often a pathologic than clinical finding, is the result of inflammatory infiltrate, hypertrophy/hyperplasia of resident cells, and possibly passive congestion.…”

Section: General Pathomechanismsmentioning

confidence: 99%

Pathologic Mechanisms Underlying the Clinical Findings in Canine Leishmaniosis due to Leishmaniainfantum/chagasi

Koutinas¹,

Koutinas

2014

Vet Pathol

129

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In dogs with symptomatic or asymptomatic leishmaniosis, Leishmania infantum appears to induce a mixed Th1/Th2 immune response that in the sick dog may eventually result in tissue damage via different pathomechanisms, notably granulomatous inflammation (eg, nodular dermatitis, osteomyelitis), immune complex deposition (eg, glomerulonephritis), and/or autoantibody production (eg, polymyositis). This is a compensatory but detrimental mechanism generated mainly because of the insufficient killing capacity of macrophages against the parasite in the susceptible dog. Clinical disease is typically exemplified as exfoliative and/or ulcerative dermatitis, with or without nasodigital hyperkeratosis and onychogryphosis, glomerulonephritis, atrophic myositis of masticatory muscles, anterior uveitis, keratoconjunctivitis sicca, epistaxis, and/or polyarthritis, appearing alone or in various combinations. The pathogenesis of these clinical conditions has recently been highlighted, to a greater or lesser extent. The usually subclinical conditions expressed as chronic colitis, chronic hepatitis, vasculitis, myocarditis, osteomyelitis, orchiepididymitis, and meningoencephalomyelitis, though uncommon, are of pathologic importance from a differential point of view. The leading cause of death among canine leishmaniosis patients is chronic proteinuric nephritis that may progress to end-stage kidney disease, nephrotic syndrome, and/or systemic hypertension. However, even the asymptomatic proteinuria, when profuse, may be a serious problem because it predisposes to arterial thromboembolism and eventually contributes to the deterioration of the body condition.

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“…A citologia fecal revelou numerosas formas amastigotas de Leishmania sp., visualizadas entre diversas bactérias, células epiteliais colunares, eritrócitos, linfócitos, macrófagos e neutrófilos (Fig. 1) et al, 2011;Ferrer et al, 1991;Silva et al, 2002;Adamama-Moraitou et al, 2007). No entanto, acreditava-se que a probabilidade de macrófagos infectados passarem para as fezes dos cães seria baixa (Pinto et al, 2012).…”

Section: Resultsunclassified