<i>Objectives</i>. Acute motor axonal neuropathy (AMAN) is a disease that leads to acute flaccid paralysis and may result from the binding of antibody and antigen to the spinal cord. The objective of this study is to evaluate the protective effect of hyperbaric oxygen treatment (HBOT) on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit. Axonal degeneration was assessed by evaluating glutathione (GSH) activity, interleukin-1<i>β</i> (IL-1<i>β</i>) expression, and clinical and histopathological features. <i>Methods</i>. Twenty-one New Zealand rabbits were divided into three groups. The treatment group was exposed to 100% oxygen at 2.4 ATA 90 minutes for 10 days at a decompression rate of 2.9 pounds per square inch/minute. GSH level was evaluated using an enzyme-linked immune-sorbent assay. An expression of IL-1<i>β</i> in the spinal cord was determined by immunohistochemistry. Clinical appearances were done by motor scale and body weight. Histological features observed neuronal swelling and inflammatory infiltration in the sagittal lumbar region and the undulation of the longitudinal sciatic nerve. <i>Results</i>. Rabbits exposed to HBO had high GSH activity levels (<span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M1" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g113-113" d="M570 304C570 398 525 448 414 448C385 448 343 445 312 434L329 511L321 518C297 504 262 482 244 460L233 411C195 397 159 381 128 358L135 332C160 347 189 360 224 373L111 -147C97 -210 84 -218 17 -231L13 -257L254 -247L259 -218L233 -216C183 -212 177 -202 189 -142L218 -1C238 -10 266 -12 283 -12C351 3 429 48 483 105C543 168 570 242 570 304ZM482 289C482 161 380 33 304 33C278 33 248 51 233 69L303 396C326 400 352 403 369 403C428 403 482 380 482 289Z"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="21.921pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 21.921 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><path id="g113-47" d="M113 -12C146 -12 170 11 170 46C170 78 146 103 114 103S58 78 58 46C58 11 82 -12 113 -12Z"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><path id="g113-54" d="M153 550H386L412 615L406 623H120L82 318C104 327 142 338 184 338C294 338 347 275 347 187C347 112 305 39 221 39C160 39 119 71 97 89C88 97 80 96 71 90C59 80 50 67 49 57C48 45 52 36 66 23C80 9 123 -12 169 -12C221 -11 288 15 342 59C403 109 431 165 431 225C431 308 366 395 238 395C212 395 165 379 127 364L153 550Z"/></g></svg>)</span></span> but unexpectedly had high IL1<i>β</i> expression (<span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M2" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><path id="g117-92" d="M512 230V281L75 514V456L453 256V254L75 55V-3L512 230Z"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="21.921pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 21.921 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-54"/></g></svg>).</span></span> In addition, the HBO-exposed rabbits had a better degree of undulation, the size of neuronal swelling was smaller, the number of macrophages was higher, and motor function was better than the AMAN model rabbits (<span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M3" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-91"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="21.921pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 21.921 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-54"/></g></svg>).</span></span> <i>Conclusions</i>. These findings indicate that HBO therapy can decrease axon degeneration by triggering GSH activity, increasing IL-1<i>β</i> level, and restoring tissues and motor status. In conclusion, HBO has a protective effect on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit.

Ni Komang Sri Dewi Untari

Kurnia Kusumastuti

Guritno Suryokusumo

I Ketut Sudiana

Protective Effect of Hyperbaric Oxygen Treatment on Axon Degeneration after Acute Motor Axonal Neuropathy

<i>Background</i>. Psoriasis is a chronic inflammatory disorder of the skin and joint, affecting nearly 2-3&#x0025; of the general population. It is assumed that imbalance between the types of natural microflora can accelerate the onset of the disease. Some fungi can play the role of superantigens and prolong chronic inflammation in the skin of psoriatic patients. The aim of the present investigation was to identify fungal species isolated from patients with psoriasis. <i>Methods</i>. From March 2016 to May 2019, 289 patients with prior diagnosis of psoriasis were included in this survey. Direct microscopy with potassium hydroxide (KOH 10&#x0025;), culture, urea hydrolysis, hair perforation test, and growth on rice grains were used to identify clinical isolates, phenotypically. For molecular identification of <i>Candida</i> species and <i>Malassezia</i> species, PCR-RFLP and PCR-sequencing were used, respectively. <i>Results</i>. Forty-six out of 289 psoriatic patients had fungal infections (15.9&#x0025;). Dermatophytes (54.3&#x0025;), <i>Candida</i> spp. (19.5&#x0025;), <i>Malassezia</i> spp. (15.2&#x0025;), <i>Aspergillus</i> spp. (6.5&#x0025;), and <i>Fusarium</i> spp. (4.3&#x0025;) were the causative agents of fungal infections. Among <i>Malassezia</i> and <i>Candida</i> species, <i>M. restricta</i> (10.8&#x0025;) and <i>C. glabrata</i> (8.7&#x0025;) were the most prevalent species, respectively. <i>Conclusion</i>. Our findings suggested that fungal pathogens, particularly dermatophytes, may play an important role in the pathogenicity of psoriasis. Also, due to the high rate of yeast colonization in the clinical samples of psoriatic patients, concomitant use of anti-inflammatory drugs and antifungals may represent an effective therapeutic approach for better management of chronic lesions among these patients. Mycological tests should be applied to indicate the incidence of fungal diseases in psoriatic patients.

Mostafa Chadeganipour

Shahla Shadzi

Rasoul Mohammadi

Fungal Infections among Psoriatic Patients: Etiologic Agents, Comorbidities, and Vulnerable Population

Fawzi Abukhalil

Ayyaz Alam Sultan

Bijal Mehta

Erin Saito

Sejal Mehta

Aaron McMurtray

Corrigendum to &#x201c;Gender and Ethnicity Based Differences in Clinical and Laboratory Features of Myasthenia Gravis&#x201d;

<i>Objectives</i>. Rheumatoid arthritis affects about 1% of the world’s population. This is a chronic autoimmune disease. It is predominant in females with progressive joint damage. Immune cells are involved, especially Th1/Th17 lymphocytes and their inflammatory cytokines. These proteins have different functions in the immune system, such as IL-16 is a chemotactic factor; IL-18 can activate NF<i>κ</i>B transcription producing inflammatory proteins; IL-31 can activate the JAK/STAT pathway which leads to the production of inflammatory factors in chronic diseases; IL-33 promotes IL-16 secretion which causes lymphocyte recruitment, and IL-32 and IL-34 appear to increase TNF secretion by macrophages activation in AR. The aim of this study was to evaluate serum levels of IL-16, IL-18, IL-31, IL-32, IL-33, and IL-34 and compare them with the severity and treatment of RA patients if there are any correlations. <i>Methods</i>. A total of 140 RA patients and 40 healthy donors were recruited from the Department of Rheumatology at Hospital das Clínicas from the Federal University of Pernambuco. 60 AR patients were naïve for any treatment. Serum cytokine levels were determined using an ELISA kit. <i>Results</i>. Serum IL-16 (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M1" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g113-113" d="M570 304C570 398 525 448 414 448C385 448 343 445 312 434L329 511L321 518C297 504 262 482 244 460L233 411C195 397 159 381 128 358L135 332C160 347 189 360 224 373L111 -147C97 -210 84 -218 17 -231L13 -257L254 -247L259 -218L233 -216C183 -212 177 -202 189 -142L218 -1C238 -10 266 -12 283 -12C351 3 429 48 483 105C543 168 570 242 570 304ZM482 289C482 161 380 33 304 33C278 33 248 51 233 69L303 396C326 400 352 403 369 403C428 403 482 380 482 289Z"/></g></svg> = 0.0491), IL-18 (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M2" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> &lt; 0.0001), IL-31 (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M3" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> = 0.0004), and IL-32 (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M4" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> = 0.0040) levels were significantly increased in RA patients compared with healthy donors. It was observed that patients using leflunomide had the lowest IL-18 levels, close to controls levels (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M5" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> = 0.0064). <i>Conclusion</i>. IL-16, IL-18, IL-31, and IL-32 are increased in the serum of RA patients. IL-18 is at lower levels in those AR who are taking leflunomide as treatment.

Pablo Ramon Gualberto Cardoso

Claudia Diniz Lopes Marques

Kamila de Melo Vilar

Andrea Tavares Dantas

Angela Luzia Branco Pinto Duarte

Ivan da Rocha Pitta

Maira Galdino da Rocha Pitta

Moacyr Jesus Barreto de Melo R&#x00EA;go

Interleukin-18 in Brazilian Rheumatoid Arthritis Patients: Can Leflunomide Reduce It?

Much public research suggests that autoimmune diseases such as rheumatoid arthritis (RA) are induced by aberrant &#x201C;self&#x201D; immune responses attacking autologous tissues and organ components. However, recent studies have reported that autoimmune diseases may be triggered by dysbiotic composition changes of the intestinal bacteria and an imbalance between these bacteria and intestinal immune systems. However, there are a few solid concepts or methods to study the putative involvement and relationship of these inner environmental factors in RA pathogenesis. Fortunately, Collagen-Induced Arthritis (CIA) and Collagen Antibody-Induced Arthritis (CAIA) models have been widely used as animal models for studying the pathogenesis of RA. In addition to RA, these models can be extensively used as animal models for studying complicated hypotheses in many diseases. In this review, we introduce some basic information about the CIA and CAIA models as well as how to apply these models effectively to investigate relationships between the pathogenesis of autoimmune diseases, especially RA, and the dysbiosis of intestinal bacterial flora.

Ryoichi Hashida

Yasunori Shimozuru

Jessica Chang

Ibis Agosto-Marlin

Takaki Waritani

Kuniaki Terato

New Studies of Pathogenesis of Rheumatoid Arthritis with Collagen-Induced and Collagen Antibody-Induced Arthritis Models: New Insight Involving Bacteria Flora

<i>Background</i>. Pernicious anemia (PA) is an autoimmune disease (AID) which is caused by lack of vitamin B12 (cobalamin) due to its impaired uptake. PA is a multifactorial disease which is associated with a number of other AID comorbidities and which is manifested as part of autoimmune polyglandular syndrome. Due to the shortage of family studies on PA, we planned to address the problem by assessing familial risks for concordant PA between family members and for discordant PA in families of other AID patients. <i>Methods</i>. We collected data on patients diagnosed with AIDs from the Swedish hospitals and family data from a population register. We calculated standardized incidence ratios (SIRs) in families for concordant and discordant risks. <i>Results</i>. The number of PA patients in the offspring generation (for which the familial risk was calculated) was 7701; 278 (3.6&#x0025;) patients had a family history of PA. The population prevalence of PA was 0.9/1000. The familial risk for PA was 3.88 when any first-degree relative was the proband, equal for men and women. The familial risk was two times higher between siblings than between offspring and parents which may be due to complex genetic background. Associations of PA with 14 discordant AIDs were significant; these included some AIDs that have previously been described as comorbidities in PA patients and several yet unreported associations, including rheumatoid arthritis and other AIDs. <i>Conclusions</i>. The familial risks for PA were high suggesting multifactorial genetic etiology. The results call for further population-level studies to unravel mechanisms of familial PA which may help to understand the etiology of this disease.

Xinjun Li

Hauke Thomsen

Kristina Sundquist

Jan Sundquist

Asta F&#xf6;rsti

Kari Hemminki

Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden

About this journal

<p><em>Autoimmune Diseases</em> publishes original research articles and&nbsp;review articles on all aspects of autoimmunity. Articles focus on the basic biology and mechanism of the disease, and medical treatment of autoimmune diseases.</p>


Journal profile

Meet the editorial board

<p><em>Autoimmune Diseases</em> maintains an Editorial Board of practicing researchers from around the world, to ensure manuscripts are handled by editors who are experts in the field of study.</p>


Editor spotlight

Submit your proposal

Do you think there is an emerging area of research that really needs to be highlighted? Or an existing research area that has been overlooked or would benefit from deeper investigation? Raise the profile of a research area by leading a Special Issue.

Special Issues

Author guidelines

Editorial board

Databases and indexing

Autoimmune Diseases - Table of contents 2021

title

Autoimmune Diseases publishes original research articles and review articles on all aspects of autoimmunity. Articles focus on the basic biology and mechanism of the disease, and medical treatment of autoimmune diseases.

Autoimmune Diseases