scholarly journals Bactericidal Effects of Low-Irradiance Low Level Light Therapy on Methicillin-Resistant Staphylococcus Aureus in Vitro

Fine Focus ◽  
2016 ◽  
Vol 2 (2) ◽  
pp. 104-115
Author(s):  
Patrick J. McMullan ◽  
Jakob Krzyston ◽  
Robert Osgood

Low Level Light Therapy (LLLT) within the visible blue spectrum (400-470 nanometers) is a well-documented therapeutic alternative to combat multidrug resistant organism infections through the generation of reactive oxygen species (ROS). However, one shortcoming of LLLT is that many studies deliver therapy through high powered lasers and lamps. High powered light sources not only require specialized staff to operate, but they also deliver the total light dose (fluence) at an exceptionally high intensity, or irradiance, which could consequently deplete the oxygen supplies required to promote LLLT’s bactericidal properties. To overcome these faults, low-irradiance LLLT, or delivering the same total fluence of LLLT over an extended period of time with decreased irradiance was evaluated in vitro. To further explore this alternative approach, the bactericidal effects of low-irradiance (10.44 mW/cm2) LLLT using wavelengths of 405-nm, 422-nm and 470-nm were studied on methicillin-resistant Staphylococcus aureus (MRSA) cultures. Among these wavelengths, it was determined that 405-nm LLLT provided the most effective reduction of bacterial load at the lowest total fluence (75 J/cm2) (94.50% reduction). The bactericidal effects of 405-nm low-irradiance LLLT were then further studied by treating MRSA cultures to 75 J/cm2 LLLT while using irradiances of 5.22 mW/cm2 and 3.48 mW/cm2. It was concluded that there was a greater reduction of MRSA bacterial load when samples were exposed to irradiances of 5.22 mW/cm2 (95.71% reduction) and 3.48 mW/cm2 (99.63% reduction). This study validates the bactericidal properties of low-irradiance LLLT on MRSA, and subsequent studies should be completed to optimize its full therapeutic potential.

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1731
Author(s):  
Yu Maw Htwe ◽  
Huashan Wang ◽  
Patrick Belvitch ◽  
Lucille Meliton ◽  
Mounica Bandela ◽  
...  

Lung endothelial dysfunction is a key feature of acute lung injury (ALI) and clinical acute respiratory distress syndrome (ARDS). Previous studies have identified the lipid-generating enzyme, group V phospholipase A2 (gVPLA2), as a mediator of lung endothelial barrier disruption and inflammation. The current study aimed to determine the role of gVPLA2 in mediating lung endothelial responses to methicillin-resistant Staphylococcus aureus (MRSA, USA300 strain), a major cause of ALI/ARDS. In vitro studies assessed the effects of gVPLA2 inhibition on lung endothelial cell (EC) permeability after exposure to heat-killed (HK) MRSA. In vivo studies assessed the effects of intratracheal live or HK-MRSA on multiple indices of ALI in wild-type (WT) and gVPLA2-deficient (KO) mice. In vitro, HK-MRSA increased gVPLA2 expression and permeability in human lung EC. Inhibition of gVPLA2 with either the PLA2 inhibitor, LY311727, or with a specific monoclonal antibody, attenuated the barrier disruption caused by HK-MRSA. LY311727 also reduced HK-MRSA-induced permeability in mouse lung EC isolated from WT but not gVPLA2-KO mice. In vivo, live MRSA caused significantly less ALI in gVPLA2 KO mice compared to WT, findings confirmed by intravital microscopy assessment in HK-MRSA-treated mice. After targeted delivery of gVPLA2 plasmid to lung endothelium using ACE antibody-conjugated liposomes, MRSA-induced ALI was significantly increased in gVPLA2-KO mice, indicating that lung endothelial expression of gVPLA2 is critical in vivo. In summary, these results demonstrate an important role for gVPLA2 in mediating MRSA-induced lung EC permeability and ALI. Thus, gVPLA2 may represent a novel therapeutic target in ALI/ARDS caused by bacterial infection.


2018 ◽  
Vol 12 (5) ◽  
pp. 45-54
Author(s):  
Ekene Ugochukwu Adim ◽  
Emeka John Dingwoke ◽  
Fatima Amin Adamude ◽  
Chidi Edenta ◽  
Ndubuisi Nwobodo Nwobodo ◽  
...  

Hernia ◽  
2006 ◽  
Vol 10 (2) ◽  
pp. 120-124 ◽  
Author(s):  
A. G. Harrell ◽  
Y. W. Novitsky ◽  
K. W. Kercher ◽  
M. Foster ◽  
J. M. Burns ◽  
...  

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