Micoplasmose respiratória murina em ratos (Rattus norvegicus): revisão de literatura

O Mycoplasma pulmonis é o agente etiológico primário da micoplasmose respiratória murina (MRM), uma importante patologia em ratos de laboratório. Os ratos são considerados ferramentas fundamentais em pesquisas experimentais há muito tempo, e ao decorrer dos anos é possível observar a sua crescente criação como animais de companhia e sua crescente presença em clínicas veterinárias. A MRM é uma patologia crônica e muitas vezes apresenta-se de maneira subclínica. Sua progressão é principalmente associada ao manejo inadequado, ressaltando a importância do conhecimento sobre os aspectos da MRM em ratos, sendo fundamental para a convivência saudável dos tutores com esses animais, além de ser uma ferramenta importante para a obtenção de resultados experimentais fidedignos.

Mast cells and pathological process in lungs of rats and mice

The aim of this study was to evaluate the number of mast cells in healthy and affected lungs of mice and rats and determine histopathological differences of the inflammatory process in the lungs of rats and mice. The lungs of healthy and affected laboratory mice (n = 80) and rats (n = 80) were used for the studies. The histpathological examination of HE slides was performed. The number of mast cells in healthy and affected lungs of mice and rats was calcaluted in Giemsa stained slides. The number of connective tissue mast cells in healthy animals and in areas of lymphoid hyperplasia and bronchiectasis was significantly higher in rats than in mice. Interstitial pneumonia with bronchiolitis and bronchiectasis and atelectasis was more expressed in rats (P = 0.006-0.025) than in mice. Lymphoid tissue hyperplasia in the lungs of mice was found much more intense than in rats (P = 0.011). In affected laboratory mice and rats Mycoplasma pulmonis was identified. Interstitial pneumonia with bronchiolitis and bronchiectasis and atelectasis were more pronounced in rats. In our opinion, because healthy rats have more mast cells in the connective lung tissue and developed more severe pneumonia, they had a higher response of mast cells to the inflammatory process compared to mice. There was a more intense lymphocytic response in the lungs of mice.

Ethmoidal meningoencephalocele in a C57BL/6J mouse

An otherwise healthy two-month-old female C57BL/6J mouse presented with a left-sided head tilt. Differential diagnoses included idiopathic necrotizing arteritis, bacterial otitis media/interna ( Pasteurella pneumotropica, Pseudomonas aeruginosa, Streptococcus sp., Mycoplasma pulmonis and Burkholderia gladioli), encephalitis, an abscess, neoplasia, a congenital malformation and an accidental or iatrogenic head trauma. Magnetic resonance imaging (MRI) revealed a large space-occupying right olfactory lobe intra-axial lesion with severe secondary left-sided subfalcine herniation. Following imaging, the animal was euthanized due to poor prognosis. Histopathologic examination revealed a unilateral, full-thickness bone defect at the base of the cribriform plate and nasal conchae dysplasia, resulting in the herniation of the olfactory bulb into the nasal cavity. There was also a left midline-shift of the frontal cortex and moderate catarrhal sinusitis in the left mandibular sinus. The MRI and histopathologic changes are consistent with a congenital malformation of the nasal cavity and frontal aspect of the skull known as an ethmoidal meningoencephalocele. Encephaloceles are rare abnormalities caused by herniation of contents of the brain through a defect in the skull which occur due to disruption of the neural tube closure at the level anterior neuropore or secondary to trauma, surgical complications, cleft palate or increased intracranial pressure. The etiology is incompletely understood but hypotheses include genetics, vitamin deficiency, teratogens, infectious agents and environmental factors. Ethmoidal encephaloceles have been reported in multiple species including humans but have not been reported previously in mice. There are multiple models for spontaneous and induced craniofacial malformation in mice, but none described for ethmoidal encephaloceles.

Prenatal infection with Mycoplasma pulmonis in rats exaggerates the angiotensin II pressor response in adult offspring

Exposure to different stressors in utero is linked to adult diseases such as obesity and hypertension. In this study, the impact of prenatal infection (PNI) on adult body weight and cardiovascular function was evaluated using a naturally occurring rodent pathogen, Mycoplasma pulmonis (MP). Pregnant Sprague-Dawley rats were infected with MP on gestational day 14 and gave birth naturally. Adult PNI offspring weighed more than controls, but resting mean arterial pressure (MAP) was unchanged. Subcutaneous injection of angiotensin II (10 μg/kg) elicited a rise in MAP that was greater in both male and female PNI offspring compared with controls ( P < 0.03). The accompanying reflex bradycardia was similar to the controls, suggesting that PNI induced baroreflex dysfunction. Subcutaneous nicotine administration, a potent cardiorespiratory stimulus, also elicited a transient rise in MAP that was generally greater in the PNI group, but the change in MAP from baseline was only significant in the PNI females compared with controls ( P < 0.03). Elevated body weight and cardiovascular reactivity in the PNI offspring was associated with an increase in the ratio of hypothalamic corticotrophin-releasing hormone receptors type 1 to type 2 gene expression in both sexes compared with controls. These findings support previous studies demonstrating that PNI induces alterations in cardiovascular function and body weight. Yet, unlike previous studies utilizing other models of PNI (e.g., endotoxin), MP PNI did not induce resting hypertension. Thus, our study provides a foundation for future studies evaluating the cardiovascular risks of offspring exposed to microbial challenges in utero.

Interleukin-17A Exacerbates Disease Severity in BALB/c Mice Susceptible to Lung Infection withMycoplasma pulmonis

ABSTRACTMycoplasmas are atypical bacteria that disrupt the immune response to promote respiratory tract infections and secondary complications. However, not every immunologic response that protects or damages the host during mycoplasma infection is known. Interleukin-17A (IL-17A) is elevated in individuals infected with mycoplasmas, but how IL-17A and its cellular sources dictate disease outcome remains unclear. Here, IL-17A is hypothesized to worsen disease in individuals susceptible to mycoplasma infection. Thus, monoclonal anti-IL-17A antibodies were given to disease-susceptible BALB/c mice and disease-resistant C57BL/6 mice infected withMycoplasma pulmonis. Neutralizing the function of IL-17A using anti-IL-17A antibodies reduced disease severity duringM. pulmonisinfection in BALB/c, but not C57BL/6, mice. Neutralizing IL-17A also reduced the incidence of neutrophilic lung lesions during infection in BALB/c mice. Reduced pathology occurred without impacting the bacterial burden, demonstrating that IL-17A is not required for mycoplasma clearance. The main source of IL-17A throughout infection in BALB/c mice was CD4+T cells, and neutralizing IL-17A after infiltration of the lungs by T cells reduced disease severity, identifying the Th17 response as a herald of late mycoplasma pathology in susceptible mice. Neutralizing IL-17A did not further reduce disease duringM. pulmonisinfection in BALB/c mice depleted of neutrophils, suggesting that IL-17A requires the presence of pulmonary neutrophils to worsen respiratory pathology. IL-17A is a pathological element of murine respiratory mycoplasma infection. Using monoclonal antibodies to neutralize IL-17A could reduce disease severity during mycoplasma infection in humans and domesticated animals.