Presently I hold an Academy Research Fellowship at the University of Helsinki. My project concentrates on analysing the role of ecological processes in affecting the interaction between environmental opportunistic pathogens (by these I mean organisms that live freely in the environment, but are able to infect host individuals upon contact) and their hosts. This work combines both theoretical analysis and microcosm experiments.

Previously, I worked as a post-doctoral fellow in a project lead by prof. Ilkka Hanski (
✝ 2016). This project concentrates on highlighting the role of the living environment on the development of atopic sensitisation in children. This work also includes analysis of the composition human microbiota and how this might relate to the regulation of the immune function. After prof. Hanski passed away, I have been in charge of this project.

After finnishing my PhD thesis and doing a short postdoc with Peter Abrams in Toronto, I started a project (postdoctoral research project, funded by the Academy of Finland) dealing with integrating spatial and temporal environmental variation in models of ecological communities. While my main research involved analysing stochastic community models, I also collaborated in research projects dealing with ecotoxicological consequences of heavy metals on chironomid communites and their bat predators, as well as testing and developing numerical methods for empirical community ecology.

My research interests include:

Community ecology
Interspecific interactions
Environmental stochasticity
– Disease ecology
– N
umerical ecology.

Past activities

2013–2015 Postdoctoral fellow in the Metapopulation Researcg Group with prof. Ilkka Hanski.

2011–2013 Postdoctoral research project funded by the Academy of Finland, considering the role of spatio-temporal environmental variation on the dynamics of metacommunities.

In 2010 I worked as a postdoctoral fellow at the university of Turku, Finland, in the project of prof. Kai Norrdahl dealing with the predictability of food web composition.

In 2009–2010 I worked at the University of Toronto, under the supervision of professors Peter Abrams & Brian Shuter, also collaborating with prof. Kevin McCann (U of Guelph). This work in Toronto dealt with food web models and the influence of climate change on spatially coupled food chains.

I did my PhD in the University of Helsinki, working in the Integrative Ecology Group, under the supervision of profs. Esa Ranta (✝ 2008) and Veijo Kaitala, and Dr. Mike Fowler. My thesis concentrated around ecological communities and the impact of environmental stochasticity on biological systems in general.

Monday, 25 September 2017

Dispersal patterns in metacommunities critically affect host-pathogen dynamics

Pathogen consumers alter spatial disease dynamics of in unexpected ways

The epidemiological dynamics of potentially free-living pathogens are often studied with respect to a specific pathogen species (e.g., cholera) and most studies concentrate only on host-pathogen interactions. Here we show that metacommunity-level interactions can alter conventional spatial disease dynamics. We introduce a pathogen eating consumer species and investigate a deterministic epidemiological model of two habitat patches, where both patches can be occupied by hosts, pathogens, and consumers of free-living pathogens. An isolated habitat patch shows periodic disease outbreaks in the host population, arising from cyclic consumer-pathogen dynamics. On the other hand, consumer dispersal between the patches generate asymmetric disease prevalence, such that the host population in one patch stays disease-free, while disease outbreaks occur in the other patch. Such asymmetry can also arise with host dispersal, where infected hosts carry pathogens to the other patch. This indirect movement of pathogens causes also a counter-intuitive effect: decreasing morbidity in a focal patch under increasing pathogen immigration. Our results underline that community-level interactions influence disease dynamics and consistent spatial asymmetry can arise also in spatially homogeneous systems. For more details, see Mononen & Ruokolainen 2017.

Monday, 17 October 2016

A mechanistic underpinning for sigmoid dose-dependent infection

Sigmoidal, dose-dependent infection: theoretical & empirical justification 

It has been proposed that biodiversity loss leads to reduced interaction between environmental and human microbiotas. Theoretical models of environmentally transmitted diseases often assume that transmission is a constant process, which scales linearly with pathogen dose. Here we question the applicability of such an assumption and propose a sigmoidal form for the pathogens infectivity response. In our formulation, this response arises under two assumptions: 1) multiple invasion events are required for a successful pathogen infection and 2) the host invasion state is reversible. The first assumption reduces pathogen infection rates at low pathogen doses, while the second assumption, due to host immune function, leads to a saturating infection rate at high doses. The derived pathogen dose:infection rate -relationship was tested against an experimental data on host mortality rates across different pathogen doses. Compared to two simpler alternatives, the sigmoidal function gave a better fit to patterns in host mortality rate (process), as well as host mortality (endpoint). Combining these alternative approaches made us more confident to conclude that the proposed model for disease transmission is theoretically sound, provides a good description of the data at hand, and is likely to be useful in developing more reliable models for infectious diseases.

A schematic illustration of a potential mechanism that gives arise to a sigmoidal infection response. In this model, each invading pathogen (with rate αP) moves the host towards the state Sn, from which the host may acquire an infection (with rate γ). Before an infection is acquired, the host immune system clears the invading pathogens (with rate β). A sigmoidal rate of infection formation requires that n > 2. See more details in: A mechanistic underpinning of sigmoid dose-dependent infection.

Tuesday, 11 October 2016

Holistic view on health: two protective layers of biodiversity

A review on the role of biodiversity in human health

The western world has witnessed a rising epidemic of chronic inflammatory disorders, such as allergies and asthma. Adoption of western lifestyles is expected to spread this epidemic also to the rest of the world, where allergies have been practically absent. In parallel, biological diversity is globally declining. This inspired Ilkka Hanski, together with medical doctors, to formulate the biodiversity hypothesis of allergic disease. This hypothesis proposes that reduced contact with natural environments, including natural microbial diversity, is associated with unhealthy human microbiota—which is less able to educate the immune system. Contact with beneficial bacteria, particularly early on in life, seems to be instrumental to the normal development of immune responses. Changes in lifestyle and diet, destruction of natural environments, and urbanisation threaten our natural exposure to these beneficial bacteria and thus also their impact on our physiology. To ensure a healthy life, we need to preserve biodiversity in the environment and make sure it finds a favourable home in us. In this review, we will focus on the role of commensal microbiota in human health and wellbeing, as well as the interaction between our microbiota and environmental microbiota, highlighting the contribution of Ilkka Hanski. 

We (humans) are protected by two nested layers of biodiversity, consisting of bacteria (and other micro-organisms) residing in our bodies (both on the external and internal surfaces) and the one surrounding us in our living environment. The diversity and composition of the inner layer is dependent on microbial colonisation from the outer layer; a process that is under the influence of our behaviour, lifestyle, environmental management, land-use planning, etc. Read more here.

Thursday, 1 September 2016

The rich and the poor: environmental biodiversity protecting from allergy

A review on the recent evidence of the biodiversity hypothesis

It has been proposed that biodiversity loss leads to reduced interaction between environmental and human microbiotas. This, in turn, may lead to immune dysfunction and impaired tolerance mechanisms in humans. That is, contact with environmental biodiversity is expected to protect from allergies. However, direct evidence linking contact with biodiversity and risk of allergy has been lacking. In this review, we consider the latest research on the biodiversity hypothesis of allergy. It is becoming clear that what you eat, drink, inhale, and touch all contribute to the grand scheme of host– microbial crosstalk that is needed for a balanced, healthy immune system to develop and maintain a healthy recognition between harmful and harmless invasions. Microbes can either communicate directly with host immune cells or affect the host via metabolism that can even lead to epigenetic modifications. Our living environment plays a key role in this process. Although especially, early exposure to diverse, beneficial microbiota from the environment is repeatedly found crucial, studies on immigrants demonstrate that condition in later life can also be decisive. We are still lacking a more detailed understanding of the interaction between natural, environmental biodiversity, and health, which calls for new innovative and more long-term investigations. The outcomes should be utilized in policy and urban planning efforts, promoting human interaction with natural biodiversity, and supporting a healthy lifestyle.

A schematic illustration of individual exposure to environmental microbial biodiversity through the course of life. See more details in The rich and the poor: environmental biodiversity protecting from allergy.