Navegando por Autor "Santiago, Helton da Costa"
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Item Coinfection with Toxoplasma gondii inhibits antigen-specific Th2 immune responses, tissue inflamation, and parasitism in BALB/c mice infected with Leishmania major.(1999) Santiago, Helton da Costa; Oliveira, Milton Adriano Pelli de; Bambirra, Eduardo Alves; Faria, Ana Maria Caetano de; Afonso, Luís Carlos Crocco; Oliveira, Leda Quercia; Gazzinelli, Ricardo TostesLesion size, cellular infiltration, and tissue parasitism in the footpads of BALB/c mice infected with Leishmania major were all dramatically inhibited during acute but not chronic infection with Toxoplasma gondii. Similarly, acute but not chronic toxoplasmosis at the time of infection with L. major had a strong inhibitory effect on development of acquired immune responses mediated by Th2 lymphocytes. In contrast, no mItem Early infection with Leishmania major restrains pathogenic response to Leishmania amazonensis and parasite growth.(2008) Lombana, Claudia Zuleida Gonzalez; Santiago, Helton da Costa; Macedo, J. P.; Rego, Virgínia Aparecida Seixas; Russo, Remo de Castro; Tafuri, Wagner Luiz; Afonso, Luís Carlos Crocco; Vieira, Leda QuerciaExperimental models of infection with Leishmania spp. have provided knowledge of several immunological events involved in the resistance mechanism used by the host to restrain parasite growth. It is well accepted that concomitant immunity exists, and there is some evidence that it would play a major role in long-lasting acquired resistance to infection. In this paper, the resistance to Leishmania amazonensis infection in C57BL/6 mice infected with Leishmania major was investigated. C57BL/6 mice, which spontaneously heal lesions caused by infection with L. major, were infected with L. amazonensis at different times before and after L. major. We demonstrated that C57BL/6 mice previously infected with L. major restrain pathogenic responses induced by L. amazonensis infection and decrease parasite burdens by one order of magnitude. Coinfected mice showed production of IFN-_ in lesions similar to mice infected solely with L. major, but higher TNF-_ and nitric oxide synthase (iNOS) mRNA expression was observed. Surprisingly, the restrained pathogenic response was not related to IL-10 production, as evidenced by lower levels of both mRNA, protein expression in lesions from co-infected mice and in co-infections in IL-10−/− mice. Examination of the inflammatory infiltrate at the site of infection showed a reduced number of monocytes and lymphocytes in L. amazonensis lesions. Additionally, differential production of the CCL3/MIP-1_ and CCL5/RANTES was observed. We suggest that the control of lesion progression caused by L. amazonensis in C57BL/6 mice pre-infected with L. major is related to the induction of a down-regulatory environment at the site of infection with L. amazonensis.Item Involvement of the chemokine RANTES (CCL5) in resistance to experimental infection with Leishmania major.(2004) Santiago, Helton da Costa; Oliveira, Carolina Ferreira; Santiago, Luciana; Ferraz, Fernanda Oliveira; Souza, Daniele da Glória de; Freitas, Luiz Antônio Rodrigues de; Afonso, Luís Carlos Crocco; Teixeira, Mauro Martins; Gazzinelli, Ricardo Tostes; Vieira, Leda QuerciaThe expression and putative role of chemokines during infection with Leishmania major in mice were investigated. CCL5 expression correlates with resistance, and blockade of CCL5 rendered mice more susceptible to infection. CCL5 is part of the cascade of events leading to efficient parasite control in L. major infection.Item A potential role of cholinergic dysfunction on Impaired Colon Motility in experimental intestinal Chagas disease.(2022) Ricci, Mayra Fernanda; Béla, Samantha Ribeiro; Barbosa, Joana Lobato; Moraes, Michele Macedo; Mazzeti, Ana Lia; Bahia, Maria Terezinha; Horta, Laila Sampaio; Santiago, Helton da Costa; Cruz, Jader dos Santos; Capettini, Luciano dos Santos Aggum; Arantes, Rosa Maria EstevesBackground/Aims Chagasic megacolon is caused by Trypanosoma cruzi, which promotes in several cases, irreversible segmental colonic dilation. This alteration is the major anatomic-clinical disorder, characterized by the enteric nervous system and muscle wall structural damage. Herein, we investigate how T. cruzi-induced progressive colonic structural changes modulate the colonic contractile pattern activity. Methods We developed a murine model of T. cruzi-infection that reproduced long-term modifications of the enlarged colon. We evaluated colonic and total intestinal transit time in animals. The patterns of motor response at several time intervals between the acute and chronic phases were evaluated using the organ bath assays. Enteric motor neurons were stimulated by electric field stimulation. The responses were analyzed in the presence of the nicotinic and muscarinic acetylcholine receptor antagonists. Western blot was performed to evaluate the expression of nicotinic and muscarinic receptors. The neurotransmitter expression was analyzed by real-time polymerase chain reaction. Results In the chronic phase of infection, there was decreased intestinal motility associated with decreased amplitude and rhythmicity of intestinal contractility. Pharmacological tests suggested a defective response mediated by acetylcholine receptors. The contractile response induced by acetylcholine was decreased by atropine in the acute phase while the lack of its action in the chronic phase was associated with tissue damage, and decreased expression of choline acetyltransferase, nicotinic subunits of acetylcholine receptors, and neurotransmitters. Conclusions T. cruzi-induced damage of smooth muscles was accompanied by motility disorders such as decreased intestinal peristalsis and cholinergic system response impairment. This study allows integration of the natural history of Chagasic megacolon motility disorders and opens new perspectives for the design of effective therapeutic.Item Splenectomy increases mortality in murine Trypanosoma cruzi infection.(2011) Maioli, Tatiani Uceli; Assis, Frankcinéia Aparecida de; Vieira, Paula Melo de Abreu; Borelli, Primavera; Santiago, Helton da Costa; Alves, Ricardo José; Romanha, Alvaro José; Carneiro, Cláudia Martins; Faria, Ana Maria Caetano deThe spleen is a secondary lymphoid organ that harbours a variety of cells such as T and B lymphocytes and antigen-presenting cells important to immune response development. In this study, we evaluated the impact of spleen removal in the immune response to experimental Trypanosoma cruzi infection. C57BL/6 mice were infected with Y strain of the parasite and infection was followed daily. Mice that underwent splenectomy had fewer parasites in peripheral blood at the peak of infection; however, mortality was increased. Histological analysis of heart and liver tissues revealed an increased number of parasites and inflammatory infiltrates at these sites. Spleen removal was associated with reduction in IFN-γ and TNF-α production during infection as well as with a decrease in specific antibody secretion. Haematological disorders were also detected. Splenectomized mice exhibited severe anaemia and decreased bone marrow cell numbers. Our results indicate that spleen integrity is critical in T. cruzi infection for the immune response against the parasite, as well as for the control of bone marrow haematological function.Item Treatment with distinct antibiotic classes causes different pulmonary outcomes on allergic airway inflammation associated with modulation of symbiotic microbiota.(2022) Cavalcante, Gregório Grama; Guimarães, Anna Gabriella; Glauss, Camila Pereira Queiroz; Pereira, Marcela Helena Gonçalves; Dias, Angélica Samer Lallo; Horta, Laila Sampaio; Oliveira, Jamil Silvano de; Cangussú, Silvia Dantas; Magalhães, Paula Prazeres; Russo, Remo de Castro; Santiago, Helton da CostaBackground. Asthma is a chronic pulmonary disease that affects about 300 million people worldwide. Previous studies have associated antimicrobial use with allergies, but the real impact of antibiotics on asthma is still elusive. We investigated the potential impact of amoxicillin (Amox), trimethoprim/sulfamethoxazole (TMP/SMX), and metronidazole (Metro) in a murine model of OVA-induced allergic airway inflammation. Methods. BALB/c mice received three cycles of 7 days of antibiotics in drinking water followed by 7 days washout and were sensitized i.p. with OVA/Alum at days 0 and 14. After the end of the last antibiotic washout, the mice were challenged with aerosolized OVA. Pulmonary parameters were evaluated, and serum, BAL, and feces were collected for analysis. Results. Amox- and TMP/SMX-treated animals displayed more severe allergic airway inflammation parameters with increased airway hyperresponsiveness, reduced lung alveolar volume, and increased levels in BAL of IL-4 and IL-6. In contrast, Metro-treated mice showed preserved FEV-50, decreased lung inflammation, and higher levels of butyrate and propionate in their feces. Metro treatment was associated with increased OVA-specific IgA in serum. BAL microbiota was abundant in allergic groups but not in nonallergic controls with the Amox-treated group displaying the increased frequency of Proteobacteria, while Metro and TMP/SMX showed increased levels of Firmicutes. In the gut, we observed the enrichment of Akkermansia muciniphila associated with reduced airway inflammation phenotype in the Metro group, even after the recovery period. Conclusion. Our data suggest that different antibiotic treatments may impact the course of experimental allergic airway inflammation in diverse ways by several mechanisms, including modulation of short-chain fat acids production by intestinal microbiota.