Lactoferrin modulates oxidative stress and inflammatory cytokines in a murine model of dysbiosis induced by clindamycin
- Inés Abad 1,2, Andrea Bellés 2,3, Ana Rodríguez-Largo 2,4, Lluís Luján 2,4, Ignacio de Blas 2,4, Dimitra Graikini 1,2, Laura Grasa 2,3,5, Lourdes Sánchez 1,2
- Inés Abad 1,2, Andrea Bellés 2,3, Ana Rodríguez-Largo 2,4
- 1Departamento de Producción Animal y Ciencia de los Alimentos, Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
- 2Instituto Agroalimentario de Aragón IA2 (UNIZAR-CITA), Zaragoza, Spain.
- 3Departamento de Farmacología, Fisiología y Medicina Legal y Forense, Facu1ltad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
- 4Departamento de Patología Animal, Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
- 5Instituto de Investigación Sanitaria de Aragón (IIS Aragón), Zaragoza, Spain.
- 0Departamento de Producción Animal y Ciencia de los Alimentos, Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
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October 8, 2024
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View abstract on PubMed
Summary
This summary is machine-generated.Clindamycin-induced intestinal dysbiosis increases protein oxidation and inflammation. Bovine lactoferrin, particularly iron-saturated lactoferrin, effectively reversed these negative effects in mice, supporting gut health.
Area Of Science
- Microbiology
- Immunology
- Biochemistry
Background
- Antibiotics like clindamycin disrupt the gut microbiota, leading to dysbiosis, reduced anti-inflammatory properties, and altered immune responses.
- Oxidative stress is a key consequence of antibiotic-induced intestinal damage.
- Lactoferrin plays a role in maintaining intestinal homeostasis and mitigating antibiotic-induced dysbiosis.
Purpose Of The Study
- To investigate the protective effects of native and iron-saturated bovine lactoferrin against clindamycin-induced intestinal dysbiosis in a murine model.
- To assess the impact of lactoferrin on oxidative stress markers and inflammatory mediator expression in the ileum.
Main Methods
- Male C57BL/6 mice were divided into six groups receiving saline, clindamycin, native lactoferrin (nLF), iron-saturated lactoferrin (sLF), nLF/clindamycin, or sLF/clindamycin.
- Analysis of lipid peroxidation and protein carbonyl content in intestinal cells.
- Quantitative real-time PCR (qRT-PCR) to determine the expression of inflammatory mediators like interleukin-6 and TNF-α.
Main Results
- Clindamycin significantly increased protein carbonyl levels (approximately 5-fold) but did not alter lipid peroxidation.
- Oral administration of iron-saturated lactoferrin (sLF) reversed the increase in protein carbonyls.
- Clindamycin elevated interleukin-6 and TNF-α expression, an effect normalized by both native (nLF) and iron-saturated lactoferrin (sLF) treatments.
Conclusions
- Bovine lactoferrin, especially the iron-saturated form, can counteract clindamycin-induced oxidative stress and inflammation in the gut.
- Lactoferrin treatment helps restore intestinal homeostasis disrupted by antibiotic-induced dysbiosis.
- These findings highlight lactoferrin's potential as a therapeutic agent to mitigate antibiotic side effects on the intestinal tract.
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