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Acute Brucella melitensis M16 infection model in mice treated with tumor necrosis factor-alpha inhibitors
Murat Kutlu1, Çağrı Ergin, Nilay Şen-Türk
1Pamukkale University, Faculty of Medicine, Denizli, Turkey. muratkutlu72@yahoo.com.
Introduction:
There is limited data in the literature about brucellosis related to an intracellular pathogen and anti-tumor necrosis factor alpha (anti-TNFα) medication. The aim of this study was to evaluate acute Brucella infections in mice receiving anti-TNFα drug treatment.
Methodology:
Anti-TNFα drugs were injected in mice on the first and fifth days of the study, after which the mice were infected with B. melitensis M16 strain. Mice were sacrificed on the fourteenth day after infection. Bacterial loads in the liver and spleen were defined, and histopathological changes were evaluated.
Results:
Neither the liver nor the spleen showed an increased bacterial load in all anti-TNFα drug groups when compared to a non-treated, infected group. The most significant histopathological findings were neutrophil infiltrations in the red pulp of the spleen and apoptotic cells with hepatocellular pleomorphism in the liver. There was no significant difference among the groups in terms of previously reported histopathological findings, such as extramedullary hematopoiesis and granuloma formation.
Conclusions:
There were no differences in hepatic and splenic bacterial load and granuloma formation, which indicate worsening of the acute Brucella infection in mice; in other words, anti-TNFα treatment did not exacerbate the acute Brucella spp. infection in mice.
Insights
Anti-tumor necrosis factor alpha (anti-TNFα) medication did not worsen acute Brucella infections in mice. Studies showed no increase in bacterial load or granuloma formation in treated mice compared to controls.
Area of Science:
- Immunology
- Infectious Diseases
- Pharmacology
Background:
- Limited data exists on brucellosis in conjunction with anti-tumor necrosis factor alpha (anti-TNFα) therapy.
- Brucellosis is an infectious disease caused by intracellular bacteria of the genus Brucella.
- Anti-TNFα medications are used to treat inflammatory conditions but may impact immune responses to infections.
Purpose of the Study:
- To investigate the effects of anti-TNFα drug treatment on acute Brucella infections.
- To evaluate bacterial loads and histopathological changes in mice receiving anti-TNFα therapy during Brucella infection.
Main Methods:
- Mice were administered anti-TNFα drugs on days 1 and 5.
- Mice were subsequently infected with Brucella melitensis M16 strain.
- Bacterial loads in the liver and spleen were quantified, and histopathological analyses were performed on day 14 post-infection.
Main Results:
- No significant increase in hepatic or splenic bacterial load was observed in anti-TNFα treated groups compared to controls.
- Histopathological examination revealed neutrophil infiltrations in the spleen and hepatocellular changes in the liver.
- No significant differences were noted in extramedullary hematopoiesis or granuloma formation among the groups.
Conclusions:
- Anti-TNFα treatment did not exacerbate acute Brucella spp. infection in mice.
- Hepatic and splenic bacterial loads and granuloma formation remained unchanged, indicating no worsening of the infection.
- This study suggests that anti-TNFα therapy may not increase susceptibility to acute Brucella infection.
