Possible Photobiomodulation on Swine Flu

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Possible Photobiomodulation on Swine Flu
Timon Cheng-Yi Liu

Thursday, 30 April 2009 10:48 UTC

Abstract

Intranasal cells and tissues play an important role in the generation of local immunity to influenza infections. It has been found that chilling caused a pronounced constriction of the blood vessels in the nose and shuts off the warm blood that supplies the white cells that fight infection so that the onset possibility of common cold symptoms increased, and hot drink provided immediate and sustained relief from symptoms of runny nose, cough, sneezing, sore throat, chilliness and tiredness. Many phenomena and the mechanism of intranasal low intensity laser therapy (ILILT) have been integrated to support the prophylaxis and rehabilitation of ILILT on swine flu in this paper.

1 Introduction

Influenza is an acute viral disease which mainly affects the respiratory tract and occurs in all age groups with yearly epidemics during the cold season. In the United States, seasonal influenza epidemics account for > 200,000 hospitalizations and > 30,000 deaths annually. More than 90% of deaths are in the elderly. A basic method of protecting the population against influenza, which is also the cheapest, is vaccination of as many people in the population as possible, especially those from high-risk patients, but it was susceptible to failure resulting from antigenic changes. Moreover, seemingly from one influenza season to the next, we have lost the use of our leading antiviral influenza drug because of resistance. Intranasal low intensity laser therapy (ILILT) (Liu et al 2009) is also extremely safe. Its possible prophylaxis and rehabilitation of on swine flu was discussed in this paper.

2 Flu pathology

Johnson et al (2005) found acute chilling of the feet causes the onset of common cold symptoms in around 10% of subjects who are chilled. Chilling of the feet in cold water (12°C ± 1°C) has been previously reported to cause an intense vasoconstriction of both the cutaneous and upper airway blood vessels (Drettner 1961) and the vasoconstriction of the upper airways has been proposed as a mechanism that reduces respiratory defence against infection (Mudd et al 1919, Eccles 2002). Chilling causes a pronounced constriction of the blood vessels in the nose and shuts off the warm blood that supplies the white cells that fight infection. When common cold viruses are circulating in the community a proportion of subjects will have sub-clinical infections, and chilling of these subjects may cause vasoconstriction in the upper airway epithelium and conversion of a sub-clinical to a clinical infection. In these cases the subject links the causality of the common cold symptoms to the chill and does not realize that they were already infected before they ‘caught’ a cold. This might be one of the causes why the individuals such as people over 65 years or under 2 years, and individuals with chronic cardiovascular, pulmonary or renal disease, diabetes mellitus or immunosuppression (Schmidt 2004) are of high risk in flu infection.
Tamura et al (1996) found that nasal Th1 cells, capable of producing the type I interferon (IFN)-gamma and mediating delayed-type hypersensitivity, a protective localized cell-mediated immune response against intracellular pathogens primarily, are involved in the type-specific acceleration of recovery from influenza after challenge in mice immunized intranasally with adjuvant-combined nucleoprotein, although the nonspecific mechanism of accelerated recovery remains to be solved. IgA is the major, if not the sole, mediator of nasal immunity to influenza virus in immunocompetent mice (Renegar et al 1991). Tamura et al (1998) also found that virus-specific IgA antibodies, produced by IgA antibody-forming cells in the nasal-associated lymphoid tissue (NALT), play an important role in recovery from infection. Therefore, NALT plays a role in the generation of local immunity to influenza infections although it is not essential for the development of protective immunity and viral clearance in the upper respiratory tract (URT) (Wiley et al 2005).
Influenza causes a broad range of illness, from symptomless infection to various respiratory syndromes and disorders affecting the heart, brain, and other organs, to fulminant primary viral and secondary bacterial pneumonia. During influenza epidemics, hospitalizations for stroke and cardiac diseases increase, and more than half of the excess mortality during such epidemics was attributed to causes other than influenza, including cardiovascular diseases and stroke (Grau et al 2005). Bogomol’tsev et al (2003) have studied microcirculation, hemocoagulation and blood viscosity in 377 of 1033 inpatients with influenza and other acute respiratory viral infections. They found that the microcirculatory changes manifest themselves with advanced erythrocyte aggregation, activation of vascular-platelet and plasmic links of hemostasis, and high blood viscosity at low shift velocities. In the presence of concomitant pathology (ischemic heart disease, hypertensive disease, diabetes mellitus) and development of complications, especially acute pneumonia, these disturbances are still greater and tend to increase to the period of decline of clinical and toxic manifestations.
The incidence of upper respiratory infections (URIs), 38% of which are due to influenza, peaks in winter (November and December). On the other hand, both acute myocardial infarction (AMI) and stroke also have their peak incidence in winter months (Meyers 2003). AMI and atherothrombotic stroke share a common pathogenesis involving disrupted atherosclerotic plaque and intravascular thrombosis. URIs result in many biochemical, cellular, and hemostatic changes that could predispose to plaque disruption and thrombosis. Infections, particularly URIs, frequently precede AMI and stroke. Up to 16% of persons older than 60 years of age experience a URI each year. Nineteen percent of those suffering an AMI recall a URI in the 2 weeks prior to their event. Three epidemiologic and one small clinical trial suggest that influenza vaccination is associated with a 50% reduction in incidence of sudden cardiac death, AMI, and ischemic stroke. Influenza vaccine is extremely safe and has a 50% efficacy.

3 Flu prophylaxis and rehabilitation

Sanu et al (2008) found that the hot drink provided immediate and sustained relief from symptoms of runny nose, cough, sneezing, sore throat, chilliness and tiredness, whereas the same drink at room temperature only provided relief from symptoms of runny nose, cough and sneezing.
IFN response represents one of the first lines of defense against influenza virus infections. Kugel et al (2008) have assessed the protective potential of exogenous IFN-alpha against seasonal and highly pathogenic influenza viruses in ferrets. Intranasal treatment with IFN-alpha several hours before infection with the H1N1 influenza A virus strain A/USSR/90/77 reduced viral titers in nasal washes at least 100-fold compared to mock-treated controls. IFN-treated animals developed only mild and transient respiratory symptoms, and the characteristic fever peak seen in mock-treated ferrets 2 days after infection was not observed. Repeated application of IFN-alpha substantially increased the protective effect of the cytokine treatment.
Fujisawa et al (1987) found that polymorphonuclear leukocytes (PMNs) (X-ray-sensitive, carrageenan-resistant) were the cells primarily responsible for early protection in influenza virus infection and that after infection with a high dose of the virus alveolar macrophages (X-ray-resistant, carrageenan-sensitive) also played a protective role in the early phase. Brokstad et al (2001) further found that the basal level of influenza-specific antibody-secreting cells in the mucosa of the respiratory tract may be important in the protection against influenza infection.
In mice administered Lactobacillus casei strain Shirota (LcS) intranasally, potent induction of interleukin 12, IFN-gamma, and tumor necrosis factor alpha, which play a very important role in excluding influenza virus (IFV), was evident in mediastinal lymph node cells. Hori et al (2001) found the titers of virus in the nasal wash of mice inoculated with 200 microg of LcS for three consecutive days (LcS 200 group) before infection were significantly (P < 0.01) lower than those of mice not inoculated with LcS (control group) (10(0.9 +/- 0.6) versus 10(2.1 +/- 1.0)) in this model of upper respiratory IFV infection, and the survival rate of the mice in the LcS 200 group was significantly (P < 0.05) greater than that of the mice in the control group (69% versus 15%). These findings suggest that intranasal administration of LcS enhances cellular immunity in the respiratory tract and protects against influenza virus infection.

4 Photobiomodulation

Photobiomodulation (PBM) is a modulation of laser irradiation or monochromatic light (LI) on biosystems, which stimulates or inhibits biological functions but does not result in irreducible damage. The LI used in PBM is always low intensity LI (LIL), ~10 mW/cm2, which is denoted as LPBM. From 1989 on, many Russian groups have studied the therapeutic effects of intranasal LIL on the local inflammation in vasomotor rhinitis and acute and chronic maxillary sinusitis. In the mainland of China, intranasal LIL has been studied to treat internal diseases and the special treatment was called intranasal low intensity laser therapy (ILILT) (Liu et al 2009). Nose-mediated therapeutics in traditional Chinese medicine (TCM) has been a very old system (Gao 1994), but ILILT began in 1998. It has been applied to treat hyperlipidemia, the blood-stasis syndrome of coronary heart disease, myocardial infarction and brain diseases such as insomnia, intractable headache, Alzheimer’s disease, Parkinson’s disease, post-stroke depression, ache in head or face, migraine, cerebral thrombosis, diabetic peripheral neuropathy, cerebral infarction, acute ischemic cerebrovascular disease, brain lesion, schizophrenia, cerebral palsy and mild cognitive impairment (Liu et al 2009). The studies indicated that serum amyloid β protein, malformation rate of erythrocytes, plasma cholecystokinin-octapeptide, the level of viscosity at lower shear rates, hematocrit, and serum lipid decreased, respectively, and melanin production, red cell deformability, superoxidase dismutase activity and β endorphin increased, respectively, circulation was improved, and immunity was regulated after ILILT (Liu et al 2009).
The vasoconstriction induced dysfunction may be improved with ILILT. Blood flow velocity and vascular diameter increased under conditions of LIL (Chertok et al 2008). Su et al (2009) have studied the therapeutic effects of ILILT on vascular diseases. 90 old patients of average age 76.1 years with coronary heart disease or cerebral infarction were randomly divided into two groups, 60 in the treatment group and 30 in the control group. The treatment group and the control group were intranasally treated with low intensity GaInP/AlGaInP diode laser irradiation at 650 nm (LGAL) at 3 and 0 mW for 30 minutes each time once a day ten days each session for two sessions, respectively. After the treatment, blood viscosity at high shear (P < 0.05), plasma viscosity (P < 0.05), red blood cell aggregation (P < 0.01), and total cholesterol (P < 0.05) decreased in the treatment group, respectively, high-density lipoprotein cholesterol increased in the treatment group (P < 0.01), but no significant differences occurred in the control group; low-density lipoprotein cholesterol, redox viscosity at low shear and high shear decreased in the treatment group (P < 0.05, 0.01 and 0,05), but increased in the control group (P < 0.001, 0.01 and 0.05 ), respectively; blood viscosity at low shear increased in the control group (P < 0.05), but no significant differences occurred in the treatment group. It was concluded that ILILT may improve blood lipid and hemorheologic behavior of patients with vascular diseases.
Moreover, there is LPBM on leukocytes (Liu et al 2009), such as its stimulating lymphocytes to produce factor(s) that can modulate endothelial cell proliferation in vitro and its modulating nitric oxide (NO) and cytokines production by leukocytes. There are two ways for PMNs to kill bacteria, phagocytosis and neutrophil extracellular traps (NETs), both of which have been found to be induced or promoted with LIL in our laboratory. Many cellular LPBM studies provide the foundation for ILILT on immunological functions so that the lymphocyte proliferation was promoted and the CD3 and CD8 increased and CD4/CD8 decreased after ILILT (Liu et al 2009). Moreover, the low intensity helium-neon laser radiation (LIHN) can induce the interferon formation from leukocytes of the donor blood (Leonova et al 1994), and induce a tumor necrosis factor-alpha (TNF- alpha) production from isolated macrophages and an INF-gamma production from isolated macrophages and splenic lymphocytes (Novoselova et al 2006).
Blood cells mediate the therapeutic effects of intranasal LPBM on the local inflammation (Liu et al 2009). The LPBM treated patients with vasomotor rhinitis showed a significant increase of T-lymphocytes and a higher capacity of T-cells to form the migration inhibition factor. For the treatment of low intensity He-Ne laser therapy on microcirculation of nasal mucosa in children with acute and chronic maxillary sinusitis, it was found that laser therapy produced a positive effect on microcirculation and reduced the potential of relapses. LPBM is effective in correction of microcirculatory disorders and tissue mechanisms of homeostasis in children with neurovegetative vasomotor rhinitis.

5 Discussion

There might be the prophylaxis of ILILT against flu. Chilling causes a pronounced constriction of the blood vessels in the nose and shuts off the warm blood that supplies the white cells that fight infection so that the onset possibility of common cold symptoms increased (Johnson et al 2005). As it is pointed out in the last section, the vasoconstriction induced dysfunction may be improved with ILILT. LIHN can induce IFN formation (Leonova et al 1994). Repeated application of IFN-alpha substantially increased the protective effect of the cytokine treatment (Kugel et al 2008). LIHN can induce a TNF- alpha production from isolated macrophages and an INF-gamma production from isolated macrophages and splenic lymphocytes (Novoselova et al 2006). The intranasal administration of LcS, potent induction of IFN-gamma and TNF-alpha, enhances cellular immunity in the respiratory tract and protects against influenza virus infection (Hori et al 2001). ILILT can rehabilitate leukocytes (Liu et al 2009). PMNs were the cells primarily responsible for early protection in influenza virus infection (Fujisawa et al 1987). The basal level of influenza-specific antibody-secreting cells in the mucosa of the respiratory tract may be important in the protection against influenza infection (Brokstad et al 2001).
The prophylaxis of ILILT against flu might hold for the high risk individuals. As the U.S. Centers for Disease Control and Prevention (CDC) (CDC 2009) has pointed out, Groups at higher risk for seasonal influenza complications include: Children less than 5 years old; Persons aged 50 years or older; Children and adolescents (aged 6 months–18 years) who are receiving long-term aspirin therapy and who might be at risk for experiencing Reye syndrome after influenza virus infection; Pregnant women; Adults and children who have chronic pulmonary, cardiovascular, hepatic, hematological, neurologic, neuromuscular, or metabolic disorders; Adults and children who have immunosuppression (including immunosuppression caused by medications or by HIV); Residents of nursing homes and other chronic-care facilities. There has been rehabilitation of ILILT on chronic cardiovascular diseases and brain diseases such as insomnia, intractable headache, Alzheimer’s disease, Parkinson’s disease, post-stroke depression, ache in head or face, migraine, cerebral thrombosis, diabetic peripheral neuropathy, cerebral infarction, acute ischemic cerebrovascular disease, brain lesion, schizophrenia, cerebral palsy and mild cognitive impairment (Liu et al 2009). There will be possible rehabilitation of ILILT on aging, chronic renal dysfunction, cancer and diabetes mellitus (Liu et al 2009). The other high-risk adults might be also treated with ILILT. For example, the immunosuppression except HIV might be treated with ILILT because ILILT can rehabilitate leukocytes (Liu et al 2009).
There might be the rehabilitation of ILILT on some flu complications. Bogomol’tsev et al (2003) found that the microcirculatory changes with influenza and other acute respiratory viral infections manifest themselves with advanced erythrocyte aggregation, activation of vascular-platelet and plasmic links of hemostasis, and high blood viscosity at low shift velocities. URIs result in many biochemical, cellular, and hemostatic changes that could predispose to plaque disruption and thrombosis and then resulted in AMI or stroke (Meyers 2003). The hot drink provided immediate and sustained relief from symptoms of runny nose, cough, sneezing, sore throat, chilliness and tiredness (Sanu et al 2008), which supports the ILILT rehabilitation.
Shortly after CDC rang the alarm bell on 21 April in a Morbidity and Mortality Weekly Report dispatch about two cases of swine flu in southern California, scientists and health officials around the world went on alert, concerned that this never-before-seen virus could lead to a killer pandemic(Cohen et al 2009). As some exports pointed out (Cohen et al 2009), the world hasn’t done nearly enough over the past 10 years to prepare for a pandemic. They worry that most countries will find themselves without access to vaccines or antiviral drugs, which could become especially dangerous if the virus causes severe disease in many people—which is still uncertain—or evolves to do so. Early on, CDC began to brew a “seed” strain for a possible vaccine against swine H1N1, and by 27 April the World Health Organization in Geneva, Switzerland, was already talking to vaccine manufacturers. One key problem is that the world’s influenza vaccine production capacity—which still relies on growing the vaccine virus in chicken eggs—is limited to some 400 million vaccine doses a year and is impossible to expand quickly (Cohen et al 2009). As to drugs, Roche, the main producer of Tamiflu, could ramp up its production capacity to some 400 million treatment courses annually fairly rapidly, and there are at least 10 generic manufacturers in addition. But the drug’s complex manufacturing process makes it too pricey for many poor nations(Cohen et al 2009). At this point, the prophylaxis and rehabilitation of ILILT might be of very important.

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Updated 01 May 2009 00:22 UTC

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