Immune responses to <i>Leptospira</i> infection: roles as biomarkers for disease severity

Various leptospiral components have been identified and shown to be involved in tissue destruction. In addition, immune responses to leptospires have been implicated in target organ damages in severe leptospirosis cases. Several inflammatory mediators were shown to be higher in susceptible animals than in resistant hosts. Moreover, cytokines/chemokines and serum proteins induced following Leptospira infection were suggested to be biomarkers for disease severity in human leptospirosis. This review focuses on the role of immune responses in the severity of leptospirosis. Studies in both animal models and humans are discussed.

Leptospirosis; Severity; Biomarker; Immune response

Authorship

Chintana Chirathaworn ^**Corresponding author at: Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10300, Thailand. E-mail address: chintana.ch@chula.ac.th (C. Chirathaworn).

Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, ThailandChulalongkorn UniversityThailandBangkok, ThailandDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand

Sutthikarn Kongpan

Master of Science Program in Medical Sciences, Faculty of Medicine, Chulalongkorn University, Bangkok, ThailandChulalongkorn UniversityThailandBangkok, ThailandMaster of Science Program in Medical Sciences, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand

Conflicts of interest

The authors declare no conflicts of interest.

*Corresponding author at: Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10300, Thailand. E-mail address: chintana.ch@chula.ac.th (C. Chirathaworn).

SCIMAGO INSTITUTIONS RANKINGS

Figures

Figures (1)

Thumbnail

Fig. 1
Diagrams suggesting how inflammatory responses involve in different disease outcomes of leptospirosis. (A) Leptospira infection in resistant animal models or in hosts with mild symptoms. Leptospira components or toxins could directly induce tissue damage. Infected hosts recognize Leptospira and respond aiming at eradicating these infectious agents. Inflammatory responses occur early and rapidly to eradicate organisms. Further tissue dissemination is prevented. Anti-inflammatory cytokines are produced to regulate inflammation. Finally, leptospires are eradicated and no or mild tissue damage is observed. (B) Leptospira infection in susceptible animal models or in hosts with severe symptoms. Leptospira components or toxins could directly induce tissue damage. There is no clear evidence demonstrating that different pathogenic Leptospira contain different virulence factors. Infected hosts recognize Leptospira and respond aiming at eradicating these infectious agents. However, in these hosts, inflammatory responses were delayed. Organisms persist and promote further inflammatory responses. The delay of Leptospira eradication may provide time for bacterial dissemination to various organs. These prolonged and massive immune response could promote further tissue damages resulting in severe organ damage observed in susceptible animals or hosts with severe clinical manifestations.

Fig. 1 Diagrams suggesting how inflammatory responses involve in different disease outcomes of leptospirosis. (A) Leptospira infection in resistant animal models or in hosts with mild symptoms. Leptospira components or toxins could directly induce tissue damage. Infected hosts recognize Leptospira and respond aiming at eradicating these infectious agents. Inflammatory responses occur early and rapidly to eradicate organisms. Further tissue dissemination is prevented. Anti-inflammatory cytokines are produced to regulate inflammation. Finally, leptospires are eradicated and no or mild tissue damage is observed. (B) Leptospira infection in susceptible animal models or in hosts with severe symptoms. Leptospira components or toxins could directly induce tissue damage. There is no clear evidence demonstrating that different pathogenic Leptospira contain different virulence factors. Infected hosts recognize Leptospira and respond aiming at eradicating these infectious agents. However, in these hosts, inflammatory responses were delayed. Organisms persist and promote further inflammatory responses. The delay of Leptospira eradication may provide time for bacterial dissemination to various organs. These prolonged and massive immune response could promote further tissue damages resulting in severe organ damage observed in susceptible animals or hosts with severe clinical manifestations.

How to cite

copy

Brazilian Society of Infectious Diseases Rua Augusto Viana, SN, 6º., 40110-060 Salvador - Bahia - Brazil, Telefax: (55 71) 3283-8172, Fax: (55 71) 3247-2756 - Salvador - BA - Brazil
E-mail: bjid@bjid.org.br

Acompanhe os números deste periódico no seu leitor de RSS

Versão para download de PDF

PDF

Inglês

Versões e tradução automática

Versão original do texto

English

Tradução automática

Google Translator
Microsoft Translator

Como citar

RIS

BIBTEX

Outros formatos de citação e exportação:

SciELO - Scientific Electronic Library Online
Rua Dr. Diogo de Faria, 1087 – 9º andar – Vila Clementino 04037-003 São Paulo/SP - Brasil
E-mail: scielo@scielo.org

Leia a Declaração de Acesso Aberto

Métricas

Immune responses to <i>Leptospira</i> infection: roles as biomarkers for disease severity

PlumX

Mensagem

[1] Conflicts of interest

The authors declare no conflicts of interest.