Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
African tick bite fever, an acute febrile illness, is caused by the obligate intracellular bacterium Rickettsia africae. Immune responses to rickettsial infections have so far mainly been investigated in vitro with infected endothelial cells as the main target cells, and in mouse models. Patient studies are rare and little is known about the immunology of human infections. In this study, inflammatory mediators and T cell responses were examined in samples from 13 patients with polymerase chain reaction-confirmed R. africae infections at different time points of illness. The Th1-associated cytokines IFNγ and IL-12 were increased in the acute phase of illness, as were levels of the T cell chemoattractant cytokine CXCL-10. In addition, the anti-inflammatory cytokine IL-10 and also IL-22 were elevated. IL-22 but not IFNγ was increasingly produced by CD4 and CD8 T cells during illness. Besides IFNγ, IL-22 appears to play a protective role in rickettsial infections.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9092931 | PMC |
http://dx.doi.org/10.1007/s00430-022-00738-5 | DOI Listing |
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