Caspase-1 Variants and Plasma IL-1β in Patients with Cutaneous Leishmaniasis in the Amazonas.

Leishmaniasis, a disease caused by protozoan spp., exhibits a broad range of clinical manifestations. Host resistance or susceptibility to infections is often influenced by the genetic make-up associated with natural immunity.

A fine mapping of single nucleotide variants and haplotype analysis of gene in patients with -cutaneous leishmaniasis and plasma cytokines IL-4, IL-5, and IL-13.

Introduction: Leishmaniasis continues to pose a substantial health burden in 97 countries worldwide. The progression and outcome of infection are influenced by various factors, including the cytokine milieu, the skin microbiota at the infection site, the specific species involved, the genetic background of the host, and the parasite load. In endemic regions to leishmaniasis, only a fraction of individuals infected actually develops the disease.

Variants of CARD8 in Leishmania guyanensis-cutaneous leishmaniasis and influence of the variants genotypes on circulating plasma cytokines IL-1β, TNFα and IL-8.

Nucleotide-binding oligomerization domain, leucine-rich repeat-containing protein family (NLR) are intracellular pathogen recognition receptors mediating innate immunity, releasing proinflammatory cytokines IL-1β and IL-18, and promoting pyroptotic cell death, upon sensing pathogenic or endogenous danger signals. In animal models, NLRP3 inflammasome has a dual role, pathogenic or protective in Leishmania-infection, depending on the Leishmania species and mice strain. Caspase recruitment containing domain 8 (CARD8) is a negative regulator of NLRP3 inflammasome and also an inhibitor of transcription factor NFĸB, a major transcription factor of proinflammatory cytokines.

Variants of NOD2 in Leishmania guyanensis-infected patients with cutaneous leishmaniasis and correlations with plasma circulating pro-inflammatory cytokines.

Leishmaniases, a group of vector-borne diseases, are caused by the protozoan intracellular parasite Leishmania (L.) and are transmitted by the phlebotomine sandflies. A wide range of clinical manifestations in L- infection is observed.

Distinct plasma chemokines and cytokines signatures in -infected patients with cutaneous leishmaniasis.

The immunopathology associated with Leishmaniasis is a consequence of inflammation. Upon infection with , the type of host-immune response is determinant for the clinical manifestations that can lead to either self-healing or chronic disease. Multiple pathways may determine disease severity.

Variants of MIRNA146A rs2910164 and MIRNA499 rs3746444 are associated with the development of cutaneous leishmaniasis caused by Leishmania guyanensis and with plasma chemokine IL-8.

Leishmania are intracellular protozoan parasites that cause a wide spectrum of clinical manifestations in genetically susceptible individuals with an insufficient or balanced Th1 immune response to eliminate the parasite. MiRNAs play important regulatory role in numerous biological processes including essential cellular functions. miR146-a acts as an inhibitor of interleukin 1 receptor associated kinase 1 (IRAK1) and tumour necrosis factor (TNF) receptor associated factor 6 (TRAF6) present in the toll-like receptors pathway while miR499a modulates TGF-β and TNF signalling pathways.

IL-23R Variant rs11805303 Is Associated With Susceptibility to the Development of Cutaneous Leishmaniasis in Leishmania guyanensis-Infected Individuals.

Background: Emerging evidence suggests that the interleukin (IL) 17/ IL-23 axis may play a role in the pathogenesis of leishmaniasis. Our aim was to investigate whether the IL-23R variant rs11805303 is a risk factor for the development of cutaneous leishmaniasis (CL) in Leishmania guyanensis-infected individuals.

Methods: We genotyped by polymerase chain reaction-restriction fragment length polymorphism the rs11805303 C/T in 828 patients with CL and 806 healthy individuals.

rs2234237 (Thr25Ser) Polymorphism in Patients with Cutaneous Leishmaniasis Caused by : A Case-Control Study in the State of Amazonas, Brazil.

Background: Leishmaniasis is an infectious disease caused by parasites. A Th1 immune response is necessary in the acute phase to control the pathogen. The triggering receptor expressed on myeloid cells (TREM)-1 is a potent amplifier of inflammation.

Epidemiology of infectious meningitis in the State of Amazonas, Brazil.

Introduction: In the State of Amazonas, particularly in the capital Manaus, meningitis has affected populations of different cultures and social strata over the years. Bacterial meningitis is caused by several different species and represents a major issue of public health importance. The present study reports the meningitis case numbers with different etiologies in Amazonas from January 1976 to December 2012.

Tegumentary leishmaniasis in the State of Amazonas: what have we learned and what do we need?

This study evaluated the occurrence of American tegumentary leishmaniasis (ATL) in the State of Amazonas, Brazil, in the last 30 years with emphasis on the last 10 years (2001 to 2010). The disease was predominantly observed in males (76.2%), in the 21- to 30-year-old age group (26.

[Record of epidemiologically important Culicidae in the rural area of Manaus, Amazonas].

The biodiversity of the Amazon region includes many species of arthropod vectors in different ecotopes, thus enabling occurrences of diseases like malaria, filariasis and arbovirosis. From August 2001 to July 2002, we gathered culicids from inside homes, from areas surrounding these homes and from forested areas of the São João Community, in the rural zone of Manaus, State of Amazonas. 1240 specimens were collected, belonging to the Culicinae (99%) and Anophelinae (1%) subfamilies, with 50 species.

[Exanthematous diseases and the first epidemic of dengue to occur in Manaus, Amazonas State, Brazil, during 1998-1999].

In 1998, the FMT/IMT-AM foundation implemented the surveillance system to diagnose acute undifferentiated febrile syndromes, with the objective of active and passive surveillance in Brazilian western Amazonian rainforest to identify and diagnose the etiologic agents of acute fever. The diagnoses were performed using serological tests to detect IgM antibodies by ELISA (Enzyme-linked-immunosorbent assay) CDC/OPAS or using commercial kits. A total of 8,557 serum samples obtained from patients with clinical suspicion of dengue virus were analyzed.

Antibody response in patients with cutaneous leishmaniasis infected by Leishmania (Viannia) braziliensis or Leishmania (Viannia) guyanensis in Brazil.

The antibody response against Leishmania (Leishmania) amazonensis crude antigen was measured through the indirect immunofluorescent assay (IFA) and the immunoenzymatic assay (ELISA) in 114 patients with cutaneous leishmaniasis (CL) in Brazil. Fifty-four patients were infected by Leishmania (Viannia) braziliensis, and 60 patients had L. (V.

[Registration of the occurrence of Aedes albopictus in an urban zone in Manaus, Amazonas, Brazil].

Information is available regarding the presence of Aedes albopictus in several municipalities of the State of Amazonas. Specimens of this mosquito species have now, for the first time, been collected from an urban area of the municipality of Manaus, Amazonas, Brazil.

[Culicidae insect fauna from rural zone in Amazonas State with incidence of sylvatic yellow fever].

After the occurrence of 14 sylvatic yellow fever cases in 10 cities in the State of Amazonas during 1996, an investigation into the presence of sylvatic yellow fever vectors was carried out. The material of larvae and adult insects was collected around residences and canopy trees within forests, using a light trap (CDC) and human bait. A total of 424 insects was collected.

Identification of antigenically distinct populations of Leishmania (Viannia) guyanensis from Manaus, Brazil, using monoclonal antibodies.

Eighty Leishmania isolates from patients who contracted cutaneous leishmaniasis in the Manaus region, Amazonas State, Brazil, were identified as Leishmania (Viannia) guyanensis by the electrophoretic profiles of six enzymes. None reacted with the species-specific monoclonal antibody B19. Two L.