Repercussion of inflammatory bowel disease on lung homeostasis: The role of photobiomodulation.

Inflammatory bowel diseases (IBD) are chronic and multifactorial diseases characterized by dysfunction of the intestinal mucosa and impaired immune response. Data show an important relationship between intestine and respiratory tract. The treatments of IBD are limited. Photobiomodulation (PBM) is an effective anti-inflammatory therapy. Our objective was to evaluate the repercussion of IBD as well as its treatment with PBM on pulmonary homeostasis. Male Wistar rats were submitted to IBD induction by acetic acid and treated or not with PBM. Rats were irradiated with red LED on both right and left sides of the ventral surface and beside the external anal region during 3 consecutive days (wavelenght 660 nm, power 100 mw, total energy 15 J and time of irradiation 150 s per point). Our results showed that IBD altered pulmonary homeostasis, since we observed an increase in the histopathological score, in myeloperoxidase activity (MPO), in mast cell degranulation, and in the release and gene expression of cytokines. We also showed that PBM treatment reduced biomarkers of IBD and reverted all augmented parameters in the lung, restoring its homeostasis. Thus, we confirm experimentally the important gut-lung axis and the role of PBM as a promising therapy.

Comparison between local abdominal and transcutaneous tail vein photobiomodulation in experimental rat model of ulcerative colitis.

Ulcerative colitis (UC) is a chronic autoimmune disease that impacts the quality of life, but current pharmacological treatments are limited. Photobiomodulation (PBM) is a light-based treatment that can be applied either locally or systemically. Here, we compare the effects of local and vascular PBM (VPBM) in an experimental rat model of UC. Male Wistar rats were induced with UC by rectal instillation of acetic acid and treated with either local abdominal PBM or VPBM to the tail vein using a 660-nm LED. The findings indicated that local PBM but not VPBM reduced intestinal histological scores. Both local and VPBM increased mucus production, decreased mast cell degranulation, and modulated TNF-α and IL-1 ß levels in the intestines. Local PBM also affected the expression of the mRNAs for IL-6, TNF-α, and IFN-γ. In conclusion, we suggest that local PBM appears to be more promising than VPBM for treating UC. However, further research is needed to fully understand the mechanisms and to optimize the parameters of PBM for UC treatment.

The impact of periodontitis in the course of chronic obstructive pulmonary disease: Pulmonary and systemic effects.

AIMS: The aim of this study was to verify the impact of periodontitis in the course of chronic obstructive pulmonary disease (COPD) in C57Bl/6J mice. MAIN METHODS: The animals were randomly divided into four groups (n = 8): Basal, Periodontitis (P), COPD and COPD+P. COPD was induced by orotracheal instillation of 30 µl of cigarette extract 3 times/week for 7 weeks. Periodontitis was induced by ligation technique for 22 days. Euthanasia was performed on 51st day. The analyzes were total/differential cells and cytokines recovered from bronchoalveolar lavage (BAL), total/differential blood cell count, platelets, total marrow cell count, airway collagen deposition, alveolar enlargement analyzed by mean linear intercept (Lm), mucus and bone crest reabsorption. One-way ANOVA followed by the Student-Newman-Keuls was used. KEY FINDINGS: The association COPD+P decreased macrophages (p = 0,0351), TNF-α (p = 0,0071) and INF-γ (p = 0,0004) in BAL, when compared to the COPD group maintaining emphysema levels by alveolar enlargement (p < .05) reorganization of collagen fibers (p = .001) and also mean linear intercept (lm) (p = .001) and mucus (p = .0001). The periodontitis group caused TNF-α increase (p = 0, 0001) in BAL. SIGNIFICANCE: Periodontitis, per se, does not alter any of the parameters analyzed, except for increased TNF-α in BAL. However, its association with COPD caused macrophages TNF-α and INF-γ alterations, when compared to the COPD group maintaining emphysema levels by alveolar enlargement and reorganization of collagen fibers. It seems that periodontitis is influencing the course of Th1 profile cell, and cytokines and pulmonary alterations. Further studies are needed to clarify the regulatory process underlying these two diseases.

The role of periodontal treatment associated with photodynamic therapy on the modulation of systemic inflammation in the experimental model of asthma and periodontitis.

BACKGROUND: The association of Periodontitis (P) with several systemic diseases, among them asthma (A), has been previously studied. As periodontal treatment (TTO) associated with photodynamic therapy (PDT) is able to treat P, the aim of this study is to verify whether periodontitis exerts systemic effects on asthma, and whether TTO, associated or not with PDT, is capable of altering the systemic course of both pathologies. METHODS: 64 male Balb/c mice were divided into 8 groups (n = 8): Basal (B), P, P + TTO, P + TTO + PDT, Asthma, A + P, A + P + TTO, A + P + TTO + PDT. After 43 days, all animals were euthanized. The total and differential leukocyte count in serum, platelet count, alveolar bronchial lavage cell count, femoral lavage cell count in addition to the reactivity of the trachea, lung edema and gingiva cytokines were analyzed. The frequency of inflammatory cells was assessed via flow cytometry. One-way ANOVA test was used, followed by the Student-Newman-Keuls post-test. RESULTS: There was an increase in the number of blood circulating eosinophils in group A when compared to group B (p < 0.01); this characterized the asthma experimental model. P (p < 0.05) presented a lower amount of cytokine TNF-α in the gingiva when compared to the Asthma group. Apart from that, there was no statistical difference found for the other analyzed parameters. CONCLUSION: These data contributed to elucidate that P and A, associated or not with TTO and PDT, are not able to interfere with the systemic parameters of Balb/c mice.

Photobiomodulation modulates the resolution of inflammation during acute lung injury induced by sepsis.

Sepsis is a big health problem and one of the most common causes of acute lung injury (ALI) leading to high mortality. Pro-resolving mediators play an important role in abrogating the inflammation and promoting tissue homeostasis restoration. ALI treatment is still a clinical health problem, so new therapies are needed. Here, we evaluated the effect of photobiomodulation treatment on the resolution process of ALI induced by lipopolysaccharide (LPS). Male Balb/c mice were submitted to LPS (ip) or vehicle and irradiated or not with light emitting diode (LED) 2 and 6 h after LPS or vehicle injection, and the parameters were investigated 3 and 7 days after the injections. Our results showed that after 3 days of LED treatment the blood and bronchoalveolar lavage (BAL) cells as well as interleukins (IL) including IL-6 and IL-17 were reduced. No differences were observed in the bone marrow cells, tracheal reactivity, and lipoxin A4 and resolvin E2. Indeed, after 7 days of LED treatment the bone marrow cells, lymphocytes, and lipoxin A4 were increased, while IL-6, IL-17, and IL-10 were decreased. No differences were observed in the blood cells and tracheal reactivity. Thus, our results showed that LED treatment attenuated ALI induced by sepsis by modulating the cell mobilization from their reserve compartments. In addition, we also showed later effects of the LED up to 7 days after the treatment. This study proposes photobiomodulation as therapeutic adjuvant to treat ALI.