Lacticaseibacillus rhamnosus modulates the inflammatory response and the subsequent lung damage in a murine model of acute lung inflammation

Objective: The present study investigated the anti-inflammatory effect of the probiotic Lacticaseibacillus rhamnosus (Lr) on lung inflammation induced by Lipopolysaccharide (LPS) of Escherichia coli in C57BL/6 mice. Methods: C57BL/6 mice were divided into four groups: control, LPS, Lr (1 day) + LPS, and Lr (14 days) + LPS. Total and differential cells from Bronchoalveolar Lavage Fluid (BALF) were counted in a Neubauer 40X chamber, and pro-and anti-inflammatory cytokines (IL-1β, IL-6, CXCL-1, TNF-α, TGF-β, and IL-10) were measured by ELISA assay. The analysis of whole leukocytes in blood was performed using the automated system Sysmex 800i. Morphometry of pulmonary tissue evaluated alveolar hemorrhage, alveolar collapse, and inflammatory cells. Pulmonary vascular permeability was assessed by Evans blue dye extravasation, and bronchoconstriction was evaluated in a tissue bath station. The transcription factor NF-kB was evaluated by ELISA, and its gene expression and TLR-2, TLR-4, MMP-9, MMP-12, and TIMP by PCR. Results: The probiotic Lr had a protective effect against the inflammatory responses induced by LPS. Lr significantly reduced pro-inflammatory cells in the airways, lung parenchyma, and blood leukocytes. Furthermore, Lr reduced the production of pro-inflammatory cytokines and chemokines in BALF and the expression of TLRs, MMPs, and NF-kB in lung tissue and maintained the expression of TIMP in treated animals promoting a protective effect on lung tissue. Conclusions: The results of the study indicate that pre-treatment with the probiotic Lr may be a promising way to mitigate lung inflammation in endotoxemia

Photobiomodulation Therapy Restores IL-10 Secretion in a Murine Model of Chronic Asthma: Relevance to the Population of CD4+CD25+Foxp3+ Cells in Lung.

It is largely known that photobiomodulation (PBM) has beneficial effects on allergic pulmonary inflammation. Our previous study showed an anti-inflammatory effect of the PBM in an acute experimental model of asthma, and we see that this mechanism is partly dependent on IL-10. However, it remains unclear whether the activation of regulatory T cells is mediated by PBM in a chronic experimental model of asthma. In this sense, the objective of this study was to verify the anti-inflammatory role of the PBM in the pulmonary inflammatory response in a chronic experimental asthma model. The protocol used for asthma induction was the administration of OVA subcutaneously (days 0 and 14) and intranasally (3 times/week, for 5 weeks). On day 50, the animals were sacrificed for the evaluation of the different parameters. The PBM used was the diode, with a wavelength of 660 nm, a power of 100 mW, and 5 J for 50 s/point, in three different application points. Our results showed that PBM decreases macrophages, neutrophils, and lymphocytes in the bronchoalveolar lavage fluid (BALF). Moreover, PBM decreased the release of cytokines by the lung, mucus, and collagen in the airways and pulmonary mechanics. When we analyzed the percentage of Treg cells in the group irradiated with laser, we verified an increase in these cells, as well as the release of IL-10 in the BALF. Therefore, we conclude that the use of PBM therapy in chronic airway inflammation attenuated the inflammatory process, as well as the pulmonary functional and structural parameters, probably due to an increase in Treg cells.post-print1951 K

Low-level laser therapy in acute pain: a systematic review of possible mechanisms of action and clinical effects in randomized placebo-controlled trials,”

ABSTRACT Objective: The aim of this study was to review the biological and clinical short-term effects of low-level laser therapy (LLLT) in acute pain from soft-tissue injury. Background Data: It is unclear if and how LLLT can reduce acute pain. Methods: Literature search of (i) controlled laboratory trials investigating potential biological mechanisms for pain relief and (ii) randomized placebo-controlled clinical trials which measure outcomes within the first 7 days after acute soft-tissue injury. Results: There is strong evidence from 19 out of 22 controlled laboratory studies that LLLT can modulate inflammatory pain by reducing levels of biochemical markers (PGE 2 , mRNA Cox 2, IL-1␤, TNF␣), neutrophil cell influx, oxidative stress, and formation of edema and hemorrhage in a dosedependent manner (median dose 7.5 J/cm 2 , range 0.3-19 J/cm 2 ). Four comparisons with non-steroidal anti-inflammatory drugs (NSAIDs) in animal studies found optimal doses of LLLT and NSAIDs to be equally effective. Seven randomized placebo-controlled trials found no significant results after irradiating only a single point on the skin overlying the site of injury, or after using a total energy dose below 5 Joules. Nine randomized placebo-controlled trials (n = 609) were of acceptable methodological quality, and irradiated three or more points and/or more than 2.5 cm 2 at site of injury or surgical incision, with a total energy of 5.0-19.5 Joules. Results in these nine trials were significantly in favor of LLLT groups over placebo groups in 15 out of 18 outcome comparisons. Poor and heterogeneous data presentation hampered statistical pooling of continuous data. Categorical data of subjective improvement were homogeneous (Q-value = 7.1) and could be calculated from four trials (n = 379) giving a significant relative risk for improvement of 2.7 (95% confidence interval [CI], 1.8-3.9) in a fixed effects model. Conclusion: LLLT can modulate inflammatory processes in a dose-dependent manner and can be titrated to significantly reduce acute inflammatory pain in clinical settings. Further clinical trials with adequate LLLT doses are needed to precisely estimate the effect size for LLLT in acute pain

Low-Level Laser Therapy Reduces Lung Inflammation in an Experimental Model of Chronic Obstructive Pulmonary Disease Involving P2X7 Receptor

Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by irreversible airflow limitation, airway inflammation and remodeling, and enlargement of alveolar spaces. COPD is in the top five leading causes of deaths worldwide and presents a high economic cost. However, there are some preventive measures to lower the risk of developing COPD. Low-level laser therapy (LLLT) is a new effective therapy, with very low cost and no side effects. So, our objective was to investigate if LLLT reduces pulmonary alterations in an experimental model of COPD. C57BL/6 mice were submitted to cigarette smoke for 75 days (2x/day). After 60 days to smoke exposure, the treated group was submitted to LLLT (diode laser, 660 nm, 30 mW, and 3 J/cm(2)) for 15 days and euthanized for morphologic and functional analysis of the lungs. Our results showed that LLLT significantly reduced the number of inflammatory cells and the proinflammatory cytokine secretion such as IL-1 beta, IL-6, and TNF-alpha in bronchoalveolar lavage fluid (BALF). We also observed that LLLT decreased collagen deposition as well as the expression of purinergic P2X7 receptor. On the other hand, LLLT increased the IL-10 release. Thus, LLLT can be pointed as a promising therapeutic approach for lung inflammatory diseases as COPD.Sao Paulo Research Foundation (FAPESP) [2012/16498-5, 2012/15165-2]FAPESP [2015/23152-6, 2014/14604-8, 2015/13486-4]Univ Nove Julho UNINOVE, Post Grad Program Biophoton Appl Hlth Sci, Sao Paulo, SP, BrazilBrazilian Inst Teaching & Res Pulm & Exercise Imm, Sao Jose Dos Campos, SP, BrazilUniv Nove Julho UNINOVE, Masters Degree & PhD Program Rehabil Sci, Expt Cardioresp Physiol Lab, Sao Paulo, SP, BrazilUniv Calif San Diego UCSD Hlth Sci, Div Trauma Surg Crit Care Burns & Acute Care Surg, Dept Surg, San Diego, CA USAFed Univ Sao Paulo UNIFESP, Inst Sci & Technol, Sao Jose Dos Campos, SP, BrazilUniv Brasil, Postgrad Program Bioengn, Sao Paulo, SP, BrazilFed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP, BrazilFed Univ Sao Paulo UNIFESP, Inst Sci & Technol, Sao Jose Dos Campos, SP, BrazilFed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP, BrazilFAPESP [2012/16498-5, 2012/15165-2]FAPESP [2015/23152-6, 2014/14604-8, 2015/13486-4]Web of Scienc

Low-level laser therapy in acute pain: a systematic review of possible mechanisms of action and clinical effects in randomized placebo-controlled trials,”

ABSTRACT Objective: The aim of this study was to review the biological and clinical short-term effects of low-level laser therapy (LLLT) in acute pain from soft-tissue injury. Background Data: It is unclear if and how LLLT can reduce acute pain. Methods: Literature search of (i) controlled laboratory trials investigating potential biological mechanisms for pain relief and (ii) randomized placebo-controlled clinical trials which measure outcomes within the first 7 days after acute soft-tissue injury. Results: There is strong evidence from 19 out of 22 controlled laboratory studies that LLLT can modulate inflammatory pain by reducing levels of biochemical markers (PGE 2 , mRNA Cox 2, IL-1␤, TNF␣), neutrophil cell influx, oxidative stress, and formation of edema and hemorrhage in a dosedependent manner (median dose 7.5 J/cm 2 , range 0.3-19 J/cm 2 ). Four comparisons with non-steroidal anti-inflammatory drugs (NSAIDs) in animal studies found optimal doses of LLLT and NSAIDs to be equally effective. Seven randomized placebo-controlled trials found no significant results after irradiating only a single point on the skin overlying the site of injury, or after using a total energy dose below 5 Joules. Nine randomized placebo-controlled trials (n = 609) were of acceptable methodological quality, and irradiated three or more points and/or more than 2.5 cm 2 at site of injury or surgical incision, with a total energy of 5.0-19.5 Joules. Results in these nine trials were significantly in favor of LLLT groups over placebo groups in 15 out of 18 outcome comparisons. Poor and heterogeneous data presentation hampered statistical pooling of continuous data. Categorical data of subjective improvement were homogeneous (Q-value = 7.1) and could be calculated from four trials (n = 379) giving a significant relative risk for improvement of 2.7 (95% confidence interval [CI], 1.8-3.9) in a fixed effects model. Conclusion: LLLT can modulate inflammatory processes in a dose-dependent manner and can be titrated to significantly reduce acute inflammatory pain in clinical settings. Further clinical trials with adequate LLLT doses are needed to precisely estimate the effect size for LLLT in acute pain

Low-level light-emitting diode therapy increases mRNA expressions of IL-10 and type I and III collagens on Achilles tendinitis in rats

The present study investigated the effects of low-level light-emitting diode (LED) therapy (880 +/- 10 nm) on interleukin (IL)-10 and type I and III collagen in an experimental model of Achilles tendinitis. Thirty male Wistar rats were separated into six groups (n = 5), three groups in the experimental period of 7 days, control group, tendinitis-induced group, and LED therapy group, and three groups in the experimental period of 14 days, tendinitis group, LED therapy group, and LED group with the therapy starting at the 7th day after tendinitis induction (LEDT delay). Tendinitis was induced in the right Achilles tendon using an intratendinous injection of 100 mu L of collagenase. the LED parameters were: optical power of 22 mW, spot area size of 0.5 cm(2), and irradiation time of 170 s, corresponding to 7.5 J/cm(2) of energy density. the therapy was initiated 12 h after the tendinitis induction, with a 48-h interval between irradiations. the IL-10 and type I and III collagen mRNA expression were evaluated by real-time polymerase chain reaction at the 7th and 14th days after tendinitis induction. the results showed that LED irradiation increased IL-10 (p < 0.001) in treated group on 7-day experimental period and increased type I and III collagen mRNA expression in both treated groups of 7- and 14-day experimental periods (p < 0.05), except by type I collagen mRNA expression in LEDT delay group. LED (880 nm) was effective in increasing mRNA expression of IL-10 and type I and III collagen. Therefore, LED therapy may have potentially therapeutic effects on Achilles tendon injuries.Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)Univ Fed Vales Jequitinhonha & Mucuri, Dept Physiotherapy, Lab Res & Anim Experimentat, BR-39100000 Diamantina, MG, BrazilUniv Camilo Castelo Branco, Inst Biomed Engn, São Paulo, BrazilInst Fed Educ Ciencia & Tecnol Sul Minas Gerais, Grp Estudos & Pesquisa Ciencias Saude, Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, UNIFESP, São Paulo, BrazilNove de Julho Univ, UNINOVE, Dept Rehabil Sci, São Paulo, BrazilUniversidade Federal de São Paulo, UNIFESP, São Paulo, BrazilFAPEMIG: APQ-01733-11Web of Scienc

Low-level laser therapy in experimental model of collagenase-induced tendinitis in rats: effects in acute and chronic inflammatory phases

A variety of treatments for tendinopathies is currently used or has been trialed. However, in fact, there is a remarkably little evidence that any conventional therapies are effective. in the last years, low-level laser therapy (LLLT) has been showing interesting results in inflammatory modulation in different musculoskeletal disorders, but the optimal parameters and mechanisms behind these effects are not fully understood. the aim of this study is to investigate if the LLLT modulates the acute and chronic phase of collagenase-induced tendinitis in rat by interfering in mRNA expression for matrix metalloproteinases (MMP13 and MMP1), vascular endothelial growth factor (VEGF), and anti-inflammatory mediator (interleukin (IL)-10). for such, tendinitis was induced by collagenase injection in male Wistar rats. Animals were treated with LLLT (780 nm, potency of 22 mW, 107 mW/cm(2), energy density of 7.5 J/cm(2), and energy delivered of 1.54 J) with different number of treatments in accordance with the inflammatory phase analyzed. LLLT was able to modulate mRNA gene expression of IL-10, VGEF, MMP1, and MMP13 both in acute than in chronic inflammatory phase (p < 0.05). Our results suggest that LLLT with parameters employed in the present study was able to modulate IL-10, VEGF, MMP1, and MMP13 mRNA gene expression both in acute than in chronic tendon inflammation. However, further studies are needed to establish optimal parameters for LLLT.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Nove de Julho Univ UNINOVE, Post Grad Program Rehabil Sci, BR-01504001 São Paulo, BrazilNove de Julho Univ UNINOVE, Post Grad Program Biophoton Appl Hlth Sci, BR-01504001 São Paulo, BrazilUniv Camilo Castelo Branco, Ctr Biomed Engn, Sao Jose Dos Campos, SP, BrazilVale Jequitinhonha & Mucuri Fed Univ, Dept Phys Therapy, Diamantina, MG, BrazilFed Univ São Paulo UNIFESP, Sao Jose Dos Campos, SP, BrazilFed Univ São Paulo UNIFESP, Sao Jose Dos Campos, SP, BrazilFAPESP: 2011/05890-9FAPESP: 2012/02087-3Web of Scienc