title: Dual Effect of low-level laser therapy (LLLT) on the acute lung inflammation induced by intestinal ischemia and reperfusion: Action on anti- and pro-inflammatory cytokines.
abstract: OBJECTIVE
  It is unknown if pro- and anti-inflammatory mediators in acute lung inflammation induced by intestinal ischemia and reperfusion (i-I/R) can be modulated by low-level laser therapy (LLLT).
  
  
  METHODS
  A controlled ex vivo study was developed in which rats were irradiated (660 nm, 30 mW, 0.08 cm² of spot size) on the skin over the right upper bronchus 1 hour post-mesenteric artery occlusion and euthanized 4 hours later. For pretreatment with anti-tumor necrosis factor (TNF) or IL-10 antibodies, the rats received either one of the agents 15 minutes before the beginning of reperfusion.
  
  
  METHODS
  Lung edema was measured by the Evans blue extravasation and pulmonary neutrophils influx was determined by myeloperoxidase (MPO) activity. Both TNF and IL-10 expression and protein in lung were evaluated by RT-PCR and ELISA, respectively.
  
  
  RESULTS
  LLLT reduced the edema (80.1 ± 41.8 µg g⁻¹  dry weight), neutrophils influx (0.83 ± 0.02 × 10⁶  cells ml⁻¹), MPO activity (2.91 ± 0.60), and TNF (153.0 ± 21.0 pg mg⁻¹  tissue) in lung when compared with respective control groups. Surprisingly, the LLLT increased the IL-10 (0.65 ± 0.13) in lung from animals subjected to i-I/R. Moreover, LLLT (0.32 ± 0.07 pg ml⁻¹) reduced the TNF-α level in RPAECs when compared with i-I/R group. The presence of anti-TNF or IL-10 antibodies did not alter the LLLT effect on IL-10 (465.1 ± 21.0 pg mg⁻¹  tissue) or TNF (223.5 ± 21.0 pg mg⁻¹ tissue) in lung from animals submitted to i-I/R.
  
  
  CONCLUSIONS
  The results indicate that the LLLT attenuates the i-I/R-induced acute lung inflammation which favor the IL-10 production and reduce TNF generation.
authors.affiliation: Research and Development Institute, Av. Shishima Hifumi, 2911, São José dos Campos, SP, Brazil. flaviafisio@hotmail.com
authors.forename: F Mafra
authors.initials: FM
authors.lastname: de Lima
authors.forename: A B
authors.initials: AB
authors.lastname: Villaverde
authors.forename: R
authors.initials: R
authors.lastname: Albertini
authors.forename: J C
authors.initials: JC
authors.lastname: Corrêa
authors.forename: R L P
authors.initials: RL
authors.lastname: Carvalho
authors.forename: E
authors.initials: E
authors.lastname: Munin
authors.forename: T
authors.initials: T
authors.lastname: Araújo
authors.forename: J A
authors.initials: JA
authors.lastname: Silva
authors.forename: F
authors.initials: F
authors.lastname: Aimbire
mesh_terms: D000208:Acute Disease; D000818:Animals; D004487:Edema; D016753:Interleukin-10 / Q000096:biosynthesis*; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000150:complications*; D054023:Lasers, Semiconductor / Q000627:therapeutic use; D028022:Low-Level Light Therapy; D008168:Lung / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D008297:Male; D009504:Neutrophils / Q000528:radiation effects; D009195:Peroxidase / Q000096:biosynthesis; D011014:Pneumonia / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000532:radiotherapy*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase