Influence of TLR-2 in the immune response in the infection induced by fungus<i>Sporothrix schenckii</i>

Negrini, Thaís de Cássia; Ferreira, Lucas Souza; Arthur, Rodrigo Alex; Alegranci, Pâmela; Placeres, Marisa Campos Polési; Spolidorio, Luís Carlos; Carlos, Iracilda Zeppone

doi:10.3109/08820139.2013.879174

Cited by 26 publications

(22 citation statements)

References 58 publications

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“…TLR9 recognizes CpG DNA in bacterial genomes (Medzhitov, 2007). To date, various investigations have reported the involvement of TLRs during infections, such as Sporothrix schenckii (TLR2), Staphylococcus aureus (TLR2), Salmonella enterica (TLR1/TLR2 complex, TLR9), Vibrio cholerae cytolysin (TLR2/TLR6 complex, TLR9) (Totemeyer et al, 2005; de C Negrini et al, 2014; Khilwani et al, 2015; Nandi and Bishayi, 2015). However, as far as we known, the association of TLRs during P. multocida infection is mainly about TLR4 to recognize P. multocida toxin (PMT) and LPS (Hildebrand et al, 2012; Kubatzky, 2012).…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis on Responses of Murine Lungs to Pasteurella multocida Infection

Qin

et al. 2017

Front. Cell. Infect. Microbiol.

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Pasteurella multocida infection in cattle causes serious epidemic diseases and leads to great economic losses in livestock industry; however, little is known about the interaction between host and P. multocida in the lungs. To explore a fully insight into the host responses in the lungs during P. multocida infection, a mouse model of Pasteurella pneumonia was established by intraperitoneal infection, and then transcriptomic analysis of infected lungs was performed. P. multocida localized and grew in murine lungs, and induced inflammation in the lungs, as well as mice death. With transcriptomic analysis, approximately 107 clean reads were acquired. 4236 differently expressed genes (DEGs) were detected during P. multocida infection, of which 1924 DEGs were up-regulated. By gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichments, 5,303 GO enrichments and 116 KEGG pathways were significantly enriched in the context of P. multocida infection. Interestingly, genes related to immune responses, such as pattern recognition receptors (PRRs), chemokines and inflammatory cytokines, were significantly up-regulated, suggesting the key roles of these genes in P. multocida infection. Transcriptomic data showed that IFN-γ/IL-17-related genes were increased, which were validated by qRT-PCR, ELISA, and immunoblotting. Our study characterized the transcriptomic profile of the lungs in mice upon Pasteurella infection, and our findings could provide valuable information with respect to better understanding the responses in mice during P. multocida infection.

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Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis on Responses of Murine Lungs to Pasteurella multocida Infection

Qin

et al. 2017

Front. Cell. Infect. Microbiol.

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“…TLR2 and TLR4), nucleotide-binding oligomerization domain-like receptors (e.g. The b-1,3-glucans are a major component of both S. schenckii and S. brasiliensis cell walls 32,33 and we and others have previously implicated TLR2 and TLR4 [33][34][35][36][37] and NLRP3 38 in Sporothrix recognition in vitro and in vivo. 6,26,27 Several kinds of bacteria/ viruses are known to directly activate NK cells through pattern recognition receptors (PRRs), especially TLR2, 28 which has been shown to be directly involved in the recognition of Mycobacterium tuberculosis by NK cells in humans and may also be involved in the NK-mediated response to human cytomegalovirus.…”

Section: Discussionmentioning

confidence: 99%

Natural killer cells are pivotal for in vivo protection following systemic infection by Sporothrix schenckii

et al. 2018

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Natural killer (NK) cells are one of the first cell types to enter inflammation sites and have been historically known as key effector cells against tumours and viruses; now, accumulating evidence shows that NK cells are also capable of direct in vitro activity and play a protective role against clinically important fungi in vivo. However, our understanding of NK cell development, maturation and activation in the setting of fungal infections is preliminary at best. Sporotrichosis is an emerging worldwide-distributed subcutaneous mycosis endemic in many countries, affecting humans and other animals and caused by various related thermodimorphic Sporothrix species, whose prototypical member is Sporothrix schenckii. We show that following systemic infection of BALB/c mice with S. schenckii sensu stricto, NK cells displayed a more mature phenotype as early as 5 days post-infection as judged by CD11b/CD27 expression. At 10 days post-infection, NK cells had increased expression of CD62 ligand (CD62L) and killer cell lectin-like receptor subfamily G member 1 (KLRG1), but not of CD25 or CD69. Depletion of NK cells with anti-asialo GM1 drastically impaired fungal clearance, leading to a more than eightfold increase in splenic fungal load accompanied by heightened systemic inflammation, as shown by augmented production of the pro-inflammatory cytokines tumour necrosis factor-α, interferon-γ and interleukin-6, but not interleukin-17A, in the spleen and serum. Our study is, to the best of our knowledge, the first to demonstrate that a fungal infection can drive NK cell maturation in vivo and that such cells are pivotal for in vivo protection against S. schenckii.

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“…CD14, CR, CD36, and galectin 3) are critical for the initial recognition and subsequent immune response against fungi displaying a PAMP profile similar to that of S. schenckii . Among these, Toll‐like receptors 2 and 4 have already been shown to have a role in the S. schenckii infection in mice . Other subsets of classical (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…18 Therefore, the recognition of S. schenckii by Toll-like receptors 2 and 4 has been associated with the induction of pro-inflammatory cytokines and other mediators. [19][20][21][22] Hence, there is a reason to believe that other PRRs participate in the host immune response against S. schenckii.…”

Section: M M U N O L O G Y O R I G I N a L A R T I C L Ementioning

confidence: 99%

“…To prevent pathogen invasion, PRRs survey the intracellular and extracellular space and play a critical role in the innate immune response by recognizing pathogen‐associated molecular patterns (PAMPs) and damage‐associated molecular patterns (DAMPs) . Therefore, the recognition of S. schenckii by Toll‐like receptors 2 and 4 has been associated with the induction of pro‐inflammatory cytokines and other mediators . Hence, there is a reason to believe that other PRRs participate in the host immune response against S. schenckii .…”

Section: Introductionmentioning

confidence: 99%

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The NLRP3 inflammasome contributes to host protection during Sporothrix schenckii infection

et al. 2017

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Sporotrichosis is a mycosis caused by fungi from the Sporothrix schenckii species complex, whose prototypical member is Sporothrix schenckii sensu stricto. Pattern recognition receptors (PRRs) recognize and respond to pathogen-associated molecular patterns (PAMPs) and shape the following adaptive immune response. A family of PRRs most frequently associated with fungal recognition is the nucleotide-binding oligomerization domain-like receptor (NLR). After PAMP recognition, NLR family pyrin domain-containing 3 (NLRP3) binds to apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and caspase-1 to form the NLRP3 inflammasome. When activated, this complex promotes the maturation of the pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18 and cell death through pyroptosis. In this study, we aimed to evaluate the importance of the NLRP3 inflammasome in the outcome of S. schenckii infection using the following three different knockout (KO) mice: NLRP3 , ASC and caspase-1 . All KO mice were more susceptible to infection than the wild-type, suggesting that NLRP3-triggered responses contribute to host protection during S. schenckii infection. Furthermore, the NLRP3 inflammasome appeared to be critical for the ex vivo release of IL-1β, IL-18 and IL-17 but not interferon-γ. Additionally, a role for the inflammasome in shaping the adaptive immune response was suggested by the lower frequencies of type 17 helper T (Th17) cells and Th1/Th17 but not Th1 cells in S. schenckii-infected KO mice. Overall, our results indicate that the NLRP3 inflammasome links the innate recognition of S. schenckii to the adaptive immune response, so contributing to protection against this infection.

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Influence of TLR-2 in the immune response in the infection induced by fungusSporothrix schenckii

Cited by 26 publications

References 58 publications

Transcriptomic Analysis on Responses of Murine Lungs to Pasteurella multocida Infection

Transcriptomic Analysis on Responses of Murine Lungs to Pasteurella multocida Infection

Natural killer cells are pivotal for in vivo protection following systemic infection by Sporothrix schenckii

The NLRP3 inflammasome contributes to host protection during Sporothrix schenckii infection

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