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                            University of Wisconsin Milwaukee
UWM Digital Commons
	August 2015
The Effects of 830nm Light on Inflammation in Retinitis Pigmentosa
	Krystal Marie Bach
		Recommended Citation
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Page 1

University of Wisconsin Milwaukee
UWM Digital Commons

Theses and Dissertations

August 2015

The Effects of 830nm Light on Inflammation in
Retinitis Pigmentosa
Krystal Marie Bach
University of Wisconsin-Milwaukee

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Recommended Citation
Bach, Krystal Marie, "The Effects of 830nm Light on Inflammation in Retinitis Pigmentosa" (2015). Theses and Dissertations. Paper
mailto:[email protected]

Page 2




Krystal M. Bach

A Thesis Submitted in

Partial Fulfillment of the

Requirements for the Degree of

Master of Science

in Biomedical Sciences


The University of Wisconsin-Milwaukee

August 2015

Page 46



I. Rationale

Much is known about the phenotypic presentations of RP and the genetic

mutations that cause it. However, very little is known about the mechanisms

responsible for the pathology of RP. Although some investigators consider the

with respect to inflammation being

involved in pathogenesis, recent studies have provided evidence that chronic

inflammation in the retina is a key factor in initiating and propagating the

degeneration of photoreceptor cells in RP (86-96). NIR light has been

demonstrated to reduce inflammation and improve visual function and

photoreceptor cell survival in several other retinopathies (97, 98, 101, 107-109).

Moreover, previous experiments using the P23H rat model of RP have

demonstrated that treatment with 830nm light significantly attenuated the loss of

visual function and photoreceptor cell degeneration (110). Since PBM has been

shown to reduce inflammation by upregulating anti-inflammatory mediators and

downregulating pro-inflammatory mediators in various conditions (104-106), it is

suspected that the modulation of cytokines and chemokines produced in the

retina is a primary mechanism by which the 830nm light reduced the severity of

disease in the P23H rat. The purpose of this experiment was to assess the effect

of the 830nm light on the concentration of inflammatory mediators found in the

P23H rat retina. However, since inflammation in this model of RP has not been

previously characterized, any differences in the retinal concentrations of the

Page 47


inflammatory mediators in the P23H rat compared to the non-dystrophic

Sprague-Dawley rat were assessed first. Characterization of the inflammatory

cytokines and chemokines associated with disease in this model may lead to

possible potential therapeutic strategies for the treatment of RP.

The retinal concentrations of the following pro-inflammatory and anti-

inflammatory mediators were determined in this study because they have been

either implicated as major immune regulators in the rat eye or shown to be

significantly elevated in other models of RP:

1) Cytokine-Induced Neutrophil Chemoattractant (CINC)-3: Also

known as MIP-2, CINC-3 is a pro-inflammatory chemokine of the CXC

subfamily. Its human analog is known as growth regulated oncogene

(GRO) of the IL-8 family. As its name suggests, CINC-3 is the primary

neutrophil chemotactic factor found in rats, resulting in the infiltration of

neutrophils at sites of inflammation. It is primarily produced by monocytes

and macrophages, but has also been shown to be produced by epithelial

cells (113, 114). Moreover, the acute intraocular inflammation caused by

endotoxin induced uveitis in Lewis rats has been associated with

increased concentrations of CINC in the serum and aqueous humor (142).

2) Interleukin (IL)- IL-1α is a pro-inflammatory cytokine produced by

macrophages and epithelial cells. It is known to cause T cell and

macrophage activation and has been shown to stimulate the production of

other pro-inflammatory factors, such as IL-1β and granulocyte-

macrophage colony stimulating factor in RPE cells (115, 116).

Page 91


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